Malcolm Needs

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We have had HFAP until they were purchased by ACHC, and both of those have cited me for the lack of correlations:  one for not performing them at all, although I pointed out that we do that on every specimen without previous records, and just last year because I didn't include crossmatch tests with my Type and Screen correlations.  I contested the citation again, stating that it was the exact same methodology as the antibody screen, but was unsuccessful as their standards say "the same test using different methodologies ".  I gave up and added XM as well.  No concept of what we do and no common sense! 

I only wish I could know another language anywhere near as well as Yanxia knows English!  She has always impressed me with her blood bank knowledge as well.

Blood bank methods aren't expected to correlate perfectly.  We use their differences to avoid rouleaux, clinically insignificant, and weak warm auto reactivity so we can better detect any significant alloantibodies. No method will detect 100% of significant antibodies. I am going to tweak the above to say we can "better detect' antibodies so it works better with the next sentence and doesn't imply that we can detect "any" significant antibodies. 

When TJC inspected us last year, we weren't cited but she recommended that we include in our QC policy for the lab why we don't do BB correlations.  I finally got around to writing this up.  Did I miss anything?  Is anything in error?
No published evidence or immunohematology expert supports periodic method correlations. Blood bank methods aren't expected to correlate perfectly.  We use their differences to avoid rouleaux, clinically insignificant, and weak warm auto reactivity so we can detect any significant alloantibodies. No method will detect 100% of significant antibodies. If they don't correlate on a given sample, there is nothing to be done to "fix" the methods. Deviation from manufacturer's instructions violates FDA and other regulations.  It would be extremely complex and probably futile to try to validate all changes that would make all specimens correlate. To select a specimen for correlation testing that is expected to correlate between methods while avoiding those that won't correlate is unscientific and a waste of resources.

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If we have to hunt for a sample to use for this that will give consistently comparable results, we aren't testing the method, we are testing our ability to find a suitable sample.  I heard that CAP will sell you one that will consistently give the same results.  If we aren't going to change anything (can't recalibrate gel!) based on the answers we get (like chemistry would), then why are we doing this?  I talked TJC out of it last inspection (I probably got a little heated over the stupidity of it because I had to come in the day after a concussion to meet with them, but maybe they took pity on me and didn't cite me because of my unfiltered brain).  No one has been able to explain to me any meaningful takeaway from doing this comparison.  If I am ever forced to do it, we will just keep copies of sample results that we run by two methods to solve a problem and make a note that they are acceptable because we expect these differences between methods.  If anyone can give me a valid use for this, I would be very appreciative.

Our Red Cross just informed us that it will discontinue providing CPDA-1 rbc.  We primarily used it to provide volume reduced red cells to pediatric patients under 3 years of age.  We will volume reduce AS-1 or AS-3 by centrifugation or washing (Terumo 2991) instead.  Probably unnecessary for most patients, but this is a long standing practice here, and it doesn't seem worthwhile trying to adjust pediatric practice in this regard.  Most patients do not need the additional volume provided by the anticoagulant-preservative in AS-1, etc., and avoiding unnecessary volume is a reasonable goal in many patients. 
There is no inherent virtue to CPDA-1 vs. AS-1 and similar solutions, and rbc preservation is slightly better in AS-1/AS-3 by in vitro metrics.  There is absolutely no factual basis for using CPD-A1 in preference to AS-1, etc. in pediatrics.  Purely expert opinion and probably unduly conservative.
 
I've attached a nice presentation by Dr. Saifee at the University of Washington, who createdAdditive solution AS-1 in Children Univ. Washington presentation Dec 2021.pptx it to educate her colleagues about using AS-1 instead of CPDA-1.
Additive solution AS-1 in Children Univ. Washington presentation Dec 2021.pptx
Pediatric RBC White Paper - November 2021.pdf

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.

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'm afraid I still can't agree with this methodology, for a couple of reasons.
Firstly, antibody/antigen reactions are, largely, governed by the Law of Mass Action.  As a result, and given a steady state of conditions (e.g. temperature), however long the incubation time may be, once a state of equilibrium is reached, there will be no net gain of antibody coating antigens, however long the incubation time may be extended.
Certainly, LISS will increase the rate of association of antibody and antigen enormously, but this will apply equally to the auto-antibody as any allo-antibody that may be present, however, of course, some antibodies will only react visibly with red cells that have homozygous expression of a particular antigen, and, if such an antibody is present, it will be very difficult to detect in the presence of an auto-antibody, but can still cause a haemolytic transfusion reaction, albeit, usually a delayed reaction, but it can still cause damage to the renal system in particular.

For these reason, I would always perform an adsorption, to get rid of the auto-antibody, even if I had no intention of performing specificity tests on the auto-antibody (although, it goes without saying, I would go all out to try to ascertain the specificity of any allo-antibody detected).

I am trying to write a book at the moment, called "Human Red Cell Serology and Blood Groups for Beginners", and Chapter 2 deals with Serological Techniques.  I attach the draft copy, which also gives relevant references, the odd diagram and abbreviations I use throughout the various chapters.
Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories.docx Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories Figures.docx Abbreviations.docx

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!!!!!!!!!!!!!!!!!!!!!!!!

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

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.

I'm afraid I still can't agree with this methodology, for a couple of reasons.
Firstly, antibody/antigen reactions are, largely, governed by the Law of Mass Action.  As a result, and given a steady state of conditions (e.g. temperature), however long the incubation time may be, once a state of equilibrium is reached, there will be no net gain of antibody coating antigens, however long the incubation time may be extended.
Certainly, LISS will increase the rate of association of antibody and antigen enormously, but this will apply equally to the auto-antibody as any allo-antibody that may be present, however, of course, some antibodies will only react visibly with red cells that have homozygous expression of a particular antigen, and, if such an antibody is present, it will be very difficult to detect in the presence of an auto-antibody, but can still cause a haemolytic transfusion reaction, albeit, usually a delayed reaction, but it can still cause damage to the renal system in particular.

For these reason, I would always perform an adsorption, to get rid of the auto-antibody, even if I had no intention of performing specificity tests on the auto-antibody (although, it goes without saying, I would go all out to try to ascertain the specificity of any allo-antibody detected).

I am trying to write a book at the moment, called "Human Red Cell Serology and Blood Groups for Beginners", and Chapter 2 deals with Serological Techniques.  I attach the draft copy, which also gives relevant references, the odd diagram and abbreviations I use throughout the various chapters.
Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories.docx Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories Figures.docx Abbreviations.docx

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'm afraid I still can't agree with this methodology, for a couple of reasons.
Firstly, antibody/antigen reactions are, largely, governed by the Law of Mass Action.  As a result, and given a steady state of conditions (e.g. temperature), however long the incubation time may be, once a state of equilibrium is reached, there will be no net gain of antibody coating antigens, however long the incubation time may be extended.
Certainly, LISS will increase the rate of association of antibody and antigen enormously, but this will apply equally to the auto-antibody as any allo-antibody that may be present, however, of course, some antibodies will only react visibly with red cells that have homozygous expression of a particular antigen, and, if such an antibody is present, it will be very difficult to detect in the presence of an auto-antibody, but can still cause a haemolytic transfusion reaction, albeit, usually a delayed reaction, but it can still cause damage to the renal system in particular.

For these reason, I would always perform an adsorption, to get rid of the auto-antibody, even if I had no intention of performing specificity tests on the auto-antibody (although, it goes without saying, I would go all out to try to ascertain the specificity of any allo-antibody detected).

I am trying to write a book at the moment, called "Human Red Cell Serology and Blood Groups for Beginners", and Chapter 2 deals with Serological Techniques.  I attach the draft copy, which also gives relevant references, the odd diagram and abbreviations I use throughout the various chapters.
Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories.docx Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories Figures.docx Abbreviations.docx

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.

When I was working on-call in a hospital laboratory, I was a lone worker.  I gave out blood, blood components and blood products without anyone checking me, apart, of course, from the patient's own immune system!

As far as I know, and I think I would, none of them had either an immediate or fatal haemolytic transfusion reaction.

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!