Malcolm Needs

I've had further thoughts upon this case (having told you not to worry about it - I live a sad life - NOT!).
It struck me that the patient has an Rh type of D+ C+ c+ E+ and e+, suggesting that the probability is that the patient has a genotype of DCe/DcE (R1R2), but this may not be the case.  She could have one of the rarer Rh genotypes, such as DCE/Dce (RzRo), DCE/dce (Rzr), Dce/dCE (Rory), etc, and this may be potentially important.
Some years ago, Joyce Poole explained to me that most grouping reagents labelled as anti-C are, in fact, a mixture of anti-c and anti-Ce, and this, she told me, included most monoclonal anti-C reagents (which surprised me, to be honest).  This is because the vast majority of the red cells transfused that stimulate an anti-C would have the haplotype of either DCe or dCe, or both, and will, therefore, also stimulate an anti-Ce.  As a result, these "hybrid" anti-C/anti-Ce reagents will react more strongly with red cells expressing the Ce compound Rh antigen (Rh7) and the C antigen (Rh2), than with red cells that only express the C (Rh2) antigen.
This would not, incidentally, explain the stronger than normal reaction with the e antigen.

However, if the patient does express one of the rarer Rh types mentioned above, say she is RzRo, she can actually produce an allo-anti-Ce, and most antibody panels only contain C+ red cells that are only Ce+ as well.  In other words, her antibody in the plasma MAY be identified as an anti-C, whereas it is actually a monospecific anti-Ce, which would neatly explain why she has an apparent anti-C.

Of course, she may also have an auto-anti-C, or a mimicking auto-anti-C (and, possibly, an allo-anti-Bg of some sort).  Sadly, for a nerd like me, I doubt if we will ever know!
I think it was John C Staley who once accused me of looking for zebras, when I hear horses hooves (I may be wrong, but I think it was John).  Anyway, this proves that he was absolutely correct about me!!!!!!!!!!!!!!!!!!!!!!!!

I am a complete antibody nerd, but, in this case, I think that you would be knocking your head against a brick wall for no reward if you try to go any further with this one.
My first thought was that it may be a case of an anti-hrB, but when I saw that the patient was a Caucasian, that was virtually "blown out of the water".  Then I saw that she had a positive DAT with anti-IgG, but not anti-Complement, and I thought Rh specificity, and, like you, I immediately thought of a mimicking auto-anti-C.  The problem is that, if you performed an elution, to actually PROVE that was the case, you would have to have access to some exceptionally rare Rh types (red cells that even many Reference Laboratories lack, let alone Hospital Laboratories).
My mentor, Joyce Poole, who taught me so much, taught me (in no uncertain terms!) not to waste such rare red cells, when I was but a young whipper snapper at the International Blood Group Reference Laboratory when it was still in London - and I'm glad she did before her boss, Carolyn Giles, needed to teach me!!!!!!!!!!!!
In this case, particularly as the patient is even older than am I, AND has been discharged, even as an antibody nerd, I would be inclined to let sleeping dogs lie!

I've had further thoughts upon this case (having told you not to worry about it - I live a sad life - NOT!).
It struck me that the patient has an Rh type of D+ C+ c+ E+ and e+, suggesting that the probability is that the patient has a genotype of DCe/DcE (R1R2), but this may not be the case.  She could have one of the rarer Rh genotypes, such as DCE/Dce (RzRo), DCE/dce (Rzr), Dce/dCE (Rory), etc, and this may be potentially important.
Some years ago, Joyce Poole explained to me that most grouping reagents labelled as anti-C are, in fact, a mixture of anti-c and anti-Ce, and this, she told me, included most monoclonal anti-C reagents (which surprised me, to be honest).  This is because the vast majority of the red cells transfused that stimulate an anti-C would have the haplotype of either DCe or dCe, or both, and will, therefore, also stimulate an anti-Ce.  As a result, these "hybrid" anti-C/anti-Ce reagents will react more strongly with red cells expressing the Ce compound Rh antigen (Rh7) and the C antigen (Rh2), than with red cells that only express the C (Rh2) antigen.
This would not, incidentally, explain the stronger than normal reaction with the e antigen.

However, if the patient does express one of the rarer Rh types mentioned above, say she is RzRo, she can actually produce an allo-anti-Ce, and most antibody panels only contain C+ red cells that are only Ce+ as well.  In other words, her antibody in the plasma MAY be identified as an anti-C, whereas it is actually a monospecific anti-Ce, which would neatly explain why she has an apparent anti-C.

Of course, she may also have an auto-anti-C, or a mimicking auto-anti-C (and, possibly, an allo-anti-Bg of some sort).  Sadly, for a nerd like me, I doubt if we will ever know!
I think it was John C Staley who once accused me of looking for zebras, when I hear horses hooves (I may be wrong, but I think it was John).  Anyway, this proves that he was absolutely correct about me!!!!!!!!!!!!!!!!!!!!!!!!

I've had further thoughts upon this case (having told you not to worry about it - I live a sad life - NOT!).
It struck me that the patient has an Rh type of D+ C+ c+ E+ and e+, suggesting that the probability is that the patient has a genotype of DCe/DcE (R1R2), but this may not be the case.  She could have one of the rarer Rh genotypes, such as DCE/Dce (RzRo), DCE/dce (Rzr), Dce/dCE (Rory), etc, and this may be potentially important.
Some years ago, Joyce Poole explained to me that most grouping reagents labelled as anti-C are, in fact, a mixture of anti-c and anti-Ce, and this, she told me, included most monoclonal anti-C reagents (which surprised me, to be honest).  This is because the vast majority of the red cells transfused that stimulate an anti-C would have the haplotype of either DCe or dCe, or both, and will, therefore, also stimulate an anti-Ce.  As a result, these "hybrid" anti-C/anti-Ce reagents will react more strongly with red cells expressing the Ce compound Rh antigen (Rh7) and the C antigen (Rh2), than with red cells that only express the C (Rh2) antigen.
This would not, incidentally, explain the stronger than normal reaction with the e antigen.

However, if the patient does express one of the rarer Rh types mentioned above, say she is RzRo, she can actually produce an allo-anti-Ce, and most antibody panels only contain C+ red cells that are only Ce+ as well.  In other words, her antibody in the plasma MAY be identified as an anti-C, whereas it is actually a monospecific anti-Ce, which would neatly explain why she has an apparent anti-C.

Of course, she may also have an auto-anti-C, or a mimicking auto-anti-C (and, possibly, an allo-anti-Bg of some sort).  Sadly, for a nerd like me, I doubt if we will ever know!
I think it was John C Staley who once accused me of looking for zebras, when I hear horses hooves (I may be wrong, but I think it was John).  Anyway, this proves that he was absolutely correct about me!!!!!!!!!!!!!!!!!!!!!!!!

I've had further thoughts upon this case (having told you not to worry about it - I live a sad life - NOT!).
It struck me that the patient has an Rh type of D+ C+ c+ E+ and e+, suggesting that the probability is that the patient has a genotype of DCe/DcE (R1R2), but this may not be the case.  She could have one of the rarer Rh genotypes, such as DCE/Dce (RzRo), DCE/dce (Rzr), Dce/dCE (Rory), etc, and this may be potentially important.
Some years ago, Joyce Poole explained to me that most grouping reagents labelled as anti-C are, in fact, a mixture of anti-c and anti-Ce, and this, she told me, included most monoclonal anti-C reagents (which surprised me, to be honest).  This is because the vast majority of the red cells transfused that stimulate an anti-C would have the haplotype of either DCe or dCe, or both, and will, therefore, also stimulate an anti-Ce.  As a result, these "hybrid" anti-C/anti-Ce reagents will react more strongly with red cells expressing the Ce compound Rh antigen (Rh7) and the C antigen (Rh2), than with red cells that only express the C (Rh2) antigen.
This would not, incidentally, explain the stronger than normal reaction with the e antigen.

However, if the patient does express one of the rarer Rh types mentioned above, say she is RzRo, she can actually produce an allo-anti-Ce, and most antibody panels only contain C+ red cells that are only Ce+ as well.  In other words, her antibody in the plasma MAY be identified as an anti-C, whereas it is actually a monospecific anti-Ce, which would neatly explain why she has an apparent anti-C.

Of course, she may also have an auto-anti-C, or a mimicking auto-anti-C (and, possibly, an allo-anti-Bg of some sort).  Sadly, for a nerd like me, I doubt if we will ever know!
I think it was John C Staley who once accused me of looking for zebras, when I hear horses hooves (I may be wrong, but I think it was John).  Anyway, this proves that he was absolutely correct about me!!!!!!!!!!!!!!!!!!!!!!!!

I am a complete antibody nerd, but, in this case, I think that you would be knocking your head against a brick wall for no reward if you try to go any further with this one.
My first thought was that it may be a case of an anti-hrB, but when I saw that the patient was a Caucasian, that was virtually "blown out of the water".  Then I saw that she had a positive DAT with anti-IgG, but not anti-Complement, and I thought Rh specificity, and, like you, I immediately thought of a mimicking auto-anti-C.  The problem is that, if you performed an elution, to actually PROVE that was the case, you would have to have access to some exceptionally rare Rh types (red cells that even many Reference Laboratories lack, let alone Hospital Laboratories).
My mentor, Joyce Poole, who taught me so much, taught me (in no uncertain terms!) not to waste such rare red cells, when I was but a young whipper snapper at the International Blood Group Reference Laboratory when it was still in London - and I'm glad she did before her boss, Carolyn Giles, needed to teach me!!!!!!!!!!!!
In this case, particularly as the patient is even older than am I, AND has been discharged, even as an antibody nerd, I would be inclined to let sleeping dogs lie!

True, but the point is, to make this joke of a requirement worthwhile, rather than just a box ticking exercise, there should be specified specificities, but they won't do that because they know (or, rather, should know) that they could never get sufficient of "weak" antibodies of certain specificities, and that diluted "strong" antibodies will have a completely different association constant, and so using these diluted "strong" antibodies will serve to control/compare absolutely nothing.

It depends what you are after.  The second edition is more about the serology of the blood groups and their respective antibodies, whereas the third edition included much more about the genes involved and how they can be tested.  They are both superb books though.

Sorry.  I never did get back to this after my holiday.

I still haven't come across a brilliant book on the subject, but four books I do like are shown below, and (sorry for being egocentric) so is one of my own lectures that touches upon the subject.




Serological Techniques for Antibody and Antigen Identification.pptx

May I ask if you are talking about positive controls or negative controls?

The reason I ask is that, if you are talking about positive controls, you should not be using R1R1 or R2R2 red cells anyway, as they have homozygous expression of the C and e, and the c and E antigens (unless, of course, they are from a donor with a VERY rare type, such as R1/D-- or R1/Rhnull).  Should you be using unit segments from a presumed R1R2 donor.  On the other hand, if you are talking about negative controls, then even if you did find it easier to get r"r or r'r units, they, of course, would have heterozygous expression of the E and e antigens, and the C and c antigens, and so would be unsuitable for negative controls for those antisera.

I'm sorry if I am sounding like I am trying to "teach my Grandmother to suck eggs" (and it is probably me getting entirely the "wrong end of the stick"), but I am totally confused.

Hey Malcolm, I especially like the bottom right quadrant that says "Date Bled".  We really need the phenotypes included on the unit face label.
 

QUITE RIGHT TOO!

So, this PROVES that CAP do not know the A from their elbow.
ALL Blood Transfusion Reference Laboratory Staff, not to mention MOST Blood Transfusion Hospital Laboratory Staff KNOW that not all antibodies can, by any means, be detected by ALL serological techniques (saline, albumin, enzyme, LISS, IAT, inhibition tests, recombinant blood group proteins, etc), let alone by ALL technologies (glass, tube, plastic tube, liquid phase microtitre plates, solid phase microtitre plates, column technologies, etc), BUT THOSE WHO RUN CAP KNOW BETTER THAN EVERYONE.

They should be thoroughly ashamed of themselves, and go back to kindergarten.

So, this PROVES that CAP do not know the A from their elbow.
ALL Blood Transfusion Reference Laboratory Staff, not to mention MOST Blood Transfusion Hospital Laboratory Staff KNOW that not all antibodies can, by any means, be detected by ALL serological techniques (saline, albumin, enzyme, LISS, IAT, inhibition tests, recombinant blood group proteins, etc), let alone by ALL technologies (glass, tube, plastic tube, liquid phase microtitre plates, solid phase microtitre plates, column technologies, etc), BUT THOSE WHO RUN CAP KNOW BETTER THAN EVERYONE.

They should be thoroughly ashamed of themselves, and go back to kindergarten.

That would be nice.  Blood centers here want to charge us for that.  They may keep it on file, but won't provide the info unless you pay... especially lookin' at you Red Cross!

I don't understand the problem.  We use the R1R1, R2R2, r'r, r"r set simply because those are most readily available/abundant from our reagent red cell sets.
C: positive control- r'r  , negative control- R2R2
c: positive control- r'r   , negative control- R1R1
E: positive control- r"r   , negative control- R1R1
e: positive control- r"r  , negative control-R2R2
I know there are other options more readily available within the general population, and likely our inventory too... but then there's a conundrum.  How do you test units you hope to use for controls without the method being QC'd in the first place?  It's a tight cycle to upkeep for a small group of generalists.  We don't have full antigen information disclosed from our blood supplier either.
Personally, I can use my own blood for several of the controls... but I don't want an extra monthly poke! Haha!

So, this PROVES that CAP do not know the A from their elbow.
ALL Blood Transfusion Reference Laboratory Staff, not to mention MOST Blood Transfusion Hospital Laboratory Staff KNOW that not all antibodies can, by any means, be detected by ALL serological techniques (saline, albumin, enzyme, LISS, IAT, inhibition tests, recombinant blood group proteins, etc), let alone by ALL technologies (glass, tube, plastic tube, liquid phase microtitre plates, solid phase microtitre plates, column technologies, etc), BUT THOSE WHO RUN CAP KNOW BETTER THAN EVERYONE.

They should be thoroughly ashamed of themselves, and go back to kindergarten.

Our window opens in October. I will not budge! If our inspector gives a deficiency for this item I will take my fight to CAP. If I do not win, then I will make the change. I am hoping by then they get their collective heads out of their posterior waste removal orifices and accept the rational and logical process.

Job security??? My comment about several of the All Common checklist items is "we ain't chemistry!". Not that it gets me anywhere.
Since we are in our inspection window, I made emergency changes to my SOP/form for that and we will scramble for suitable specimens.   Our problem is finding enough suitable antibodies with sufficient sample volume to do all this extra testing. As part of our Patient Blood Management program we draw minimal patient specimens - just enough to do the ABS and an antibody ID if it isn't a warm auto workup. We can squeak extra antibody screens out if the patients Hgb is low enough, but not multiple ID panels. My only solution to that is to do abbreviated panels using 3 Ag positive cells and 3 Ag negative cells, then state that the results are consistent with the antibody IDed with solid phase. If that's not good enough - (bad words). 

QUITE RIGHT TOO!

So, this PROVES that CAP do not know the A from their elbow.
ALL Blood Transfusion Reference Laboratory Staff, not to mention MOST Blood Transfusion Hospital Laboratory Staff KNOW that not all antibodies can, by any means, be detected by ALL serological techniques (saline, albumin, enzyme, LISS, IAT, inhibition tests, recombinant blood group proteins, etc), let alone by ALL technologies (glass, tube, plastic tube, liquid phase microtitre plates, solid phase microtitre plates, column technologies, etc), BUT THOSE WHO RUN CAP KNOW BETTER THAN EVERYONE.

They should be thoroughly ashamed of themselves, and go back to kindergarten.

QUITE RIGHT TOO!

So, this PROVES that CAP do not know the A from their elbow.
ALL Blood Transfusion Reference Laboratory Staff, not to mention MOST Blood Transfusion Hospital Laboratory Staff KNOW that not all antibodies can, by any means, be detected by ALL serological techniques (saline, albumin, enzyme, LISS, IAT, inhibition tests, recombinant blood group proteins, etc), let alone by ALL technologies (glass, tube, plastic tube, liquid phase microtitre plates, solid phase microtitre plates, column technologies, etc), BUT THOSE WHO RUN CAP KNOW BETTER THAN EVERYONE.

They should be thoroughly ashamed of themselves, and go back to kindergarten.

QUITE RIGHT TOO!

So, this PROVES that CAP do not know the A from their elbow.
ALL Blood Transfusion Reference Laboratory Staff, not to mention MOST Blood Transfusion Hospital Laboratory Staff KNOW that not all antibodies can, by any means, be detected by ALL serological techniques (saline, albumin, enzyme, LISS, IAT, inhibition tests, recombinant blood group proteins, etc), let alone by ALL technologies (glass, tube, plastic tube, liquid phase microtitre plates, solid phase microtitre plates, column technologies, etc), BUT THOSE WHO RUN CAP KNOW BETTER THAN EVERYONE.

They should be thoroughly ashamed of themselves, and go back to kindergarten.