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Questions about a potential A subgroup


AmyL86

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Hi, think this is my first post here. My name is Amy, just to share a tidbit with everyone.. 

 

I had a patient today that typed as such:

 

Forward type:

Anti-A = 2+

Anti-B = 4+

Anti-D = 4+

 

Reverse type:

Acell = 0

Bcell = 0

 

Anti-A1 = 0

 

87 y/o male, oncology patient. 

 

I was reviewing reports for the BB Supervisor, when I saw the weak Anti-A in forward, I investigated and got the aforementioned results.

The overnight tech released A+ blood on this patient, but no symptoms of transfusion reaction.

I notified my pathologist and switched the patient to O+ in light of the absence of A1 antigens.

 

my question:

I am surprised to see that the A cell in the reverse type is coming up negative. In my texbook, type discrepancies such as this are accompanied by the presence of anti-A1 in the patient's plasma. Here, I don't have a demostrable Anti-A1 and I am wondering if the antibody is naturally occuring, and in what frequency?

 

 

 

 

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Hi Amy,

My first thought was, why did the overnight person give group A blood, rather than group AB? But, perhaps you do not carry group AB in your stock.

Between 1 and 2% of the random White and Black population are A2B, and of those, only 25% produce an anti-A1. An anti-A1 that is clinically significant (reacts at 37oC) is disappearingly rare, so I wouldn't worry about it, but why switch to group O?

The ABO antigens are not direct gene products, but are the result of the action of transferase enzymes that ARE direct gene products (give or take a bit of post-translational jiggery pokery!) and the A transferase and the B transferase compete with one another to put their own terminal sugar residues on to the Type 1 and Type 2 backbones, and it is not unusual for the A antigen to be weaker than the B (so that an A1 reacts more strongly with anti-A than does an A1B, and an A2 reacts more strongly with anti-A than does an A2B).

This patient is also an elderly oncology patient, and both age and his condition can affect the expression of ABO antigens.

I would switch back to group A for transfusion if I were you (or, better still, AB).

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  • 1 year later...

Hi Amy, welcome to the site by the way. I ditto what Mary and Malcolm said. He could also be an A3B. A2B or A3B, he should also show reactivity with anti-H. I would not consider this a typing discrepancy as your front and backtype match; the reagent anti-A is just a bit weaker than expected. In any event, there is absolutely no reason not to give him AB. Give him enough A1B, and you might even get that anti-A reaction up to 3 or 4+! 

 

Phil

Edited by Dr. Pepper
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  • 2 months later...
On ‎2‎/‎4‎/‎2014 at 1:10 AM, Malcolm Needs said:

Hi Amy,

My first thought was, why did the overnight person give group A blood, rather than group AB? But, perhaps you do not carry group AB in your stock.

Between 1 and 2% of the random White and Black population are A2B, and of those, only 25% produce an anti-A1. An anti-A1 that is clinically significant (reacts at 37oC) is disappearingly rare, so I wouldn't worry about it, but why switch to group O?

The ABO antigens are not direct gene products, but are the result of the action of transferase enzymes that ARE direct gene products (give or take a bit of post-translational jiggery pokery!) and the A transferase and the B transferase compete with one another to put their own terminal sugar residues on to the Type 1 and Type 2 backbones, and it is not unusual for the A antigen to be weaker than the B (so that an A1 reacts more strongly with anti-A than does an A1B, and an A2 reacts more strongly with anti-A than does an A2B).

This patient is also an elderly oncology patient, and both age and his condition can affect the expression of ABO antigens.

I would switch back to group A for transfusion if I were you (or, better still, AB).

Hi Malcolm. Happy Holidays to you and family. The results given appear to suggest an A variant; with no Anti A1. Usually group A donor packed red blood cells are actually A1. Despite probable immune compromise of this patient would transfusion with group A packed red blood cells not be contraindicated? Would O packed cells not be the better choice here?

Edited by rravkin@aol.com
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27 minutes ago, rravkin@aol.com said:

Hi Malcolm. Happy Holidays to you and family. The results given appear to suggest an A variant; with no Anti A1. Usually group A donor packed red blood cells are actually A1. Despite probable immune compromise of this patient would transfusion with group A packed red blood cells not be contraindicated? Would O packed cells not be the better choice here?

Hi Ronald,

Thank you, and the same to you and your family.  I hope you had a wonderful Christmas and I hope you have a Happy and Prosperous New Year.

In answer to your question, I agree that the results appear to show a potential subgroup of A, but that does not mean that the patient requires group O blood.  As I said in my original post, if there is no anti-A1 present, certainly no anti-A1 that is reacting at strictly 37oC, there is no reason why the patient should not receive group A blood; even group A1 blood (or, in this case, group A1B blood).

Why do I say this?

Well, there will be no clinical sequelae if A1B blood is given, in the same way that, we often give group A1 blood to a patient who is also A1, but who has auto-anti-H, auto-anti-I or auto-anti-HI, knowing full well that both the H and the I antigens will be expressed on the red cells of this blood, rather than giving either Oh or adult ii blood (and, as far as I am aware Oh adult ii in combination does not exist - or, at least, has not yet been described), because we know that there will not be any nasty consequences.

In this case, we can give A1B blood, with no worries, and in doing so, can conserve group O blood for those patients who cannot be given any other ABO type; namely group O patients.

I must stress that, in no way am I saying that group O packed red cells could not be used in this situation (of course, they most certainly could be); all I am saying is that there is no clinical reason why precious group O red cells should be given above giving group A1B (in this case) units.

Do you see what I mean?  If not, tell me and I will try to explain it in a different way.

Best wishes,

Malcolm

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13 hours ago, Malcolm Needs said:

Hi Ronald,

Thank you, and the same to you and your family.  I hope you had a wonderful Christmas and I hope you have a Happy and Prosperous New Year.

In answer to your question, I agree that the results appear to show a potential subgroup of A, but that does not mean that the patient requires group O blood.  As I said in my original post, if there is no anti-A1 present, certainly no anti-A1 that is reacting at strictly 37oC, there is no reason why the patient should not receive group A blood; even group A1 blood (or, in this case, group A1B blood).

Why do I say this?

Well, there will be no clinical sequelae if A1B blood is given, in the same way that, we often give group A1 blood to a patient who is also A1, but who has auto-anti-H, auto-anti-I or auto-anti-HI, knowing full well that both the H and the I antigens will be expressed on the red cells of this blood, rather than giving either Oh or adult ii blood (and, as far as I am aware Oh adult ii in combination does not exist - or, at least, has not yet been described), because we know that there will not be any nasty consequences.

In this case, we can give A1B blood, with no worries, and in doing so, can conserve group O blood for those patients who cannot be given any other ABO type; namely group O patients.

I must stress that, in no way am I saying that group O packed red cells could not be used in this situation (of course, they most certainly could be); all I am saying is that there is no clinical reason why precious group O red cells should be given above giving group A1B (in this case) units.

Do you see what I mean?  If not, tell me and I will try to explain it in a different way.

Best wishes,

Malcolm

Hi Malcolm,

Thank for your good wishes. For this case, I think I understand what you are saying as far as the patient not demonstrating the A1 antibody at this time but this patient is most likely immune compromised for two reaesons;  elderly, and under cancer treatment; so perhaps this is why there is no antibody. But then, there is the question of potential to produce this Anti A1. Does this patient have that potential to produce an Anti A1 at a later time?

And then with respect to the issue of inventory management, type O Pos is far more readily available (at least in the Northeast Section of the US) then AB; as a matter of fact in our current inventory, we have over twenty times more O Pos PC's then AB PC's. So the O cells are readily available.

As far as the Oh example, the Bombay phenotype, if I'm not mistaken; with respect to the described recipient phenotype, this donor would be ideal if the Oh type was not so rare.

I would agree with the pathologist in this case and give O PC's, at least until there is some resolve with the cancer and/or treatment and then repeat the Type and Screen later when the patient is more immune competent, and go from there.

But then I do not recall why this patient was in need of blood in the first place; is the need theropeutic or is the patient actively bleeding. The reason for the need could also impact the chioce of ABO type.

 

 

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11 hours ago, rravkin@aol.com said:

For this case, I think I understand what you are saying as far as the patient not demonstrating the A1 antibody at this time but this patient is most likely immune compromised for two reaesons;  elderly, and under cancer treatment; so perhaps this is why there is no antibody. But then, there is the question of potential to produce this Anti A1. Does this patient have that potential to produce an Anti A1 at a later time?

And then with respect to the issue of inventory management, type O Pos is far more readily available (at least in the Northeast Section of the US) then AB; as a matter of fact in our current inventory, we have over twenty times more O Pos PC's then AB PC's. So the O cells are readily available.

As far as the Oh example, the Bombay phenotype, if I'm not mistaken; with respect to the described recipient phenotype, this donor would be ideal if the Oh type was not so rare.

I would agree with the pathologist in this case and give O PC's, at least until there is some resolve with the cancer and/or treatment and then repeat the Type and Screen later when the patient is more immune competent, and go from there.

But then I do not recall why this patient was in need of blood in the first place; is the need theropeutic or is the patient actively bleeding. The reason for the need could also impact the chioce of ABO type.

 

 

Hi Ronald,

As the patient gives a negative result with anti-A1 grouping reagent, there is, roughly speaking, a 25% chance that they may make an anti-A1 (see my original post), but a 75% chance that they will not!  Even if the patient is amongst the 25% of A2B individuals who do produce an anti-A1, the chances of him making an anti-A1 that can be detected at strictly 37oC are miniscual, as anti-A1 is usually weak and IgM.  However, let me give you another thought to reflect upon.

The patient may also be either M or N negative.  He may be S or s negative.  He may be P1 negative.  He is probably Lu(a-).  He is probably Kp(a-) and Js(a-).  He may be Fy(a-) or Fy(b-).  He may be Jk(a-) or Jk(b-).  He may even be Le(a-b-).  Would you perform a "full red cell type" to see which of these red cell antigens are not expressed on his red cells, and then give antigen negative blood, just in case he makes an antibody to any of the missing antigens (and remember, many of these are much more immunogenic than is the A1 antigen when transfused to an A2 individual, and some of the antibodies can be far more clinically significant than an anti-A1)?????!!!!!!!!!  I have my doubts!

You are, of course, absolutely correct when you say that an 87-year-old patient is very much less likely to make an antibody than is a younger patient, as is an oncology patient of any age - which means that this particular patient is very unlikely to make an anti-A1!!!!!

Again, I agree with you that any hospital's inventory is likely to have many times more group O units than AB units, BUT, I would ask why this is so?  The answer is two-fold.  The first is that there are many more group O individuals in the donor pool, than AB individuals.  It follows, therefore, that, as we all know, there are many times more group O patients than there are group AB patients.  If these group O units are given (willy nilly) to all patients, there will be insufficient units of group O blood for group O patients who actually cannot be given any other ABO group (except, of course, Oh).  I am not saying that group O blood was given to this patient in a willy nilly fashion; but what I am saying is that it was unnecessary so to do, when he could have been given either group AB or group A blood, with no clinical risk.

Yes, of course I agree that Oh would be the best blood to give in the scenario I put forward, and yes, the reason it is not given is that it is so rare, but I was also pointing out that we freely give H Positive blood under such circumstances, with no clinically significant sequalae; in other words, exactly like giving group A1B or group A1 packed red cells in this case.

I, therefore, profoundly disagree with the pathologist's decision in this case.

I can't recall the circumstances in which the blood was requested (except that it was requested at night).

It would be great if amyL86 would let us know if the patient has now produced an anti-A1 as a result of the blood given overnight.  I am prepared to bet a large amount of money that he has not so done!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

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20 hours ago, Malcolm Needs said:

Hi Ronald,

As the patient gives a negative result with anti-A1 grouping reagent, there is, roughly speaking, a 25% chance that they may make an anti-A1 (see my original post), but a 75% chance that they will not!  Even if the patient is amongst the 25% of A2B individuals who do produce an anti-A1, the chances of him making an anti-A1 that can be detected at strictly 37oC are miniscual, as anti-A1 is usually weak and IgM.  However, let me give you another thought to reflect upon.

The patient may also be either M or N negative.  He may be S or s negative.  He may be P1 negative.  He is probably Lu(a-).  He is probably Kp(a-) and Js(a-).  He may be Fy(a-) or Fy(b-).  He may be Jk(a-) or Jk(b-).  He may even be Le(a-b-).  Would you perform a "full red cell type" to see which of these red cell antigens are not expressed on his red cells, and then give antigen negative blood, just in case he makes an antibody to any of the missing antigens (and remember, many of these are much more immunogenic than is the A1 antigen when transfused to an A2 individual, and some of the antibodies can be far more clinically significant than an anti-A1)?????!!!!!!!!!  I have my doubts!

You are, of course, absolutely correct when you say that an 87-year-old patient is very much less likely to make an antibody than is a younger patient, as is an oncology patient of any age - which means that this particular patient is very unlikely to make an anti-A1!!!!!

Again, I agree with you that any hospital's inventory is likely to have many times more group O units than AB units, BUT, I would ask why this is so?  The answer is two-fold.  The first is that there are many more group O individuals in the donor pool, than AB individuals.  It follows, therefore, that, as we all know, there are many times more group O patients than there are group AB patients.  If these group O units are given (willy nilly) to all patients, there will be insufficient units of group O blood for group O patients who actually cannot be given any other ABO group (except, of course, Oh).  I am not saying that group O blood was given to this patient in a willy nilly fashion; but what I am saying is that it was unnecessary so to do, when he could have been given either group AB or group A blood, with no clinical risk.

Yes, of course I agree that Oh would be the best blood to give in the scenario I put forward, and yes, the reason it is not given is that it is so rare, but I was also pointing out that we freely give H Positive blood under such circumstances, with no clinically significant sequalae; in other words, exactly like giving group A1B or group A1 packed red cells in this case.

I, therefore, profoundly disagree with the pathologist's decision in this case.

I can't recall the circumstances in which the blood was requested (except that it was requested at night).

It would be great if amyL86 would let us know if the patient has now produced an anti-A1 as a result of the blood given overnight.  I am prepared to bet a large amount of money that he has not so done!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Hi Malcolm,

I agree with you that there is probably an unlikely possibility that this patient will develop and Anti A1 and any other antibody to the more antigenic antigen systems at present and perhaps in the future as well given the great

probability of a state of immune compromise. (I would also like to ask you if you know of any studies that address when an immune compromised patient would regain immune competence; I know there are probably many variables to be considered.)

I also agree that the probability of being sensitized to another antigen system is probably greater, and this risk is a general possibility any time any patient is transfused. But I would still agree with the pathologist in transfusing O Pos PC's because we know that there is already the general risk of sensitization to the A1 antigen and even though an Anti A1 may not be as harmful as other antibodies, why add an additional 25% percent of risk.

I also think that perhaps this pathologist may not be as expert as you and is therefore covering their bases.

But, Malcolm, I also wanted to wish you and your family the happiest of New Years and my best wishes,

Ronald

PS I can see molecular testing used more regularly on the horizon with all of it's benefits and liabilities.

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Dear Roland

I would like to totally agree with what Malcolm said above.  You are worrying about anti-A1 for nothing.  There is no risk.  If you think that the possibility of developing anti-A1 is a 'risk', then you should seriously consider doing a complete phenotype, confirming that with genotype, and then match blood 100% for all antigens.  Overkill?  Yes, of course it is.  but so is worrying about anti-A1.  If you want to use your group O blood because it's easier for your stock control, fine, but there's really NO scientific reason for doing this.

And actually - in this case, molecular testing would be an expensive unnecessary.

anna

 

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  • 3 weeks later...
On ‎1‎/‎1‎/‎2016 at 0:29 PM, galvania said:

Dear Roland

I would like to totally agree with what Malcolm said above.  You are worrying about anti-A1 for nothing.  There is no risk.  If you think that the possibility of developing anti-A1 is a 'risk', then you should seriously consider doing a complete phenotype, confirming that with genotype, and then match blood 100% for all antigens.  Overkill?  Yes, of course it is.  but so is worrying about anti-A1.  If you want to use your group O blood because it's easier for your stock control, fine, but there's really NO scientific reason for doing this.

And actually - in this case, molecular testing would be an expensive unnecessary.

anna

 

Hi Anna,

I have been giving this situation much thought and I think that we are speaking about practical and theoretical issues. Lets look at another immune compromised population, the neonate. If we have a neonate with an Rh typing of Negative or undetermined  we would, in practice give Rh Negative red cells. However, we know that the immune competence of the neonate is well documented and that the neonate can not generate an immune response and therefore can not produce an Anti D if we were to give Rh Positive red cells; and for sake of argument, not considering any maternal influences. However, we know that normally the neonate immune system has the capability to produce antibodies after three to four months of life; at, or greater than, the three month RBC circulating life cycle; therefore the neonate, theoretically, if give Rh Positive red cells would most likely not develop an Anti D. With respect to this case, which as I said, is also, most probably, immune compromised for two reasons, we do not know when this patient may become immune competent, unlike the Neonate, and therefore, more practical to give type O red cells.

I hope this lends some clarification.:)

Also, my name is Ronald but Roland is a good derivative.

Edited by rravkin@aol.com
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On ‎1‎/‎18‎/‎2016 at 2:13 AM, galvania said:

Dear Ronald

Sorry about giving you a new name.

No - you cannot compare the two.  There is an absolutely major difference.  Anti-D is a highly clinically significant antibody Anti-A1 is absolutely not.

anna

Galvania,

Thank you for your post but I was not trying to compare reaction strength; I was more focused on antibody prevention. That is the comparison; both the neonate and our patient here are part of immune suppressed populations.

With respect to the neonate we know that the suppression is really a lack of development of the immune system and that in three to four months the immune will be competent and capable of producing antibodies when sensitized. Our patient is also immune suppressed for two reasons, elderly and under treatment for cancer. The difference from the neonate is that we do not know when, if ever, our patient will become immune competent. Furthermore the immune competency in general may not be fully understood at all about our patient but given the age and treatment of our patient the better blood product is that which will not add any additional risk in antibody production.

I practice and believe that part of our work in supplying compatible blood products is not only to identify an antibody but also to reduce the risk of producing an antibody as well; this reduction in risk of antibody production can circumvent complications in compatibility testing as well as any in-vivo complications, either acute or delayed. I firmly believe that this is the logic of the pathologist in switching to type O red cells in this case.

These types of issues maybe resolved if and when molecular testing becomes more affordable; but I am sure this testing will lead to other discussions as well.

 

And if you do not mind, Cliff, Malcom, Galvania and everyone, I would like to ask you to take a moment of silence in condolence for the passing of Glen Frye, one of the founding members of the Eagles, and know that his passing along with the passing of David Bowie last week are just happy an sad reminders that none of us are getting any younger and that we should take a moment to sit back and appreciate our lives and our privileges, especially this site and our ability to communicate and exchange ideas. :):)  

 

Edited by rravkin@aol.com
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Dear Ronald

I never mentioned reaction strength.  What I said was that anti-D is a clinically relevant antibody (i.e. it can cause HDN and transfusion reactions), whereas anti-A1 is not.  And I repeat (from a previous post) giving A1 blood to an A2 patient, immunocompromised or not, does NOT constitute a risk, and therefore does not need to be avoided

anna

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23 hours ago, galvania said:

Dear Ronald

I never mentioned reaction strength.  What I said was that anti-D is a clinically relevant antibody (i.e. it can cause HDN and transfusion reactions), whereas anti-A1 is not.  And I repeat (from a previous post) giving A1 blood to an A2 patient, immunocompromised or not, does NOT constitute a risk, and therefore does not need to be avoided

anna

Dear Galvania,

I searched "Anti A1 Clinical Relevance" and found two articles. The first is on the site, Blood Bank Guy, posted 2012 and completed agrees with your and Malcom's statement that Anti A1 is clinically insignificant in the majority of cases. It also states that information on the production of Anti A1 antibodies is "sparse;" and it gives disclaimer at the bottom of the post entered by Monica Lasarre in 2012.

The second site I saw was from PubMed.gov, US National Library of Medicine, National Institutes of Health, an Abstract from 2009 by Daskova NG, Ragimos AA, and Asoskova TK where they state that " The risk of the development of post transfusion reactions or complications is particularly great when Anti A1 antibodies are active at 37C and belong to the IgG class. They go on to suggest donors of O RBC's or BRBC's for recipients that are type A2B, which our 87yr old oncology patient appears to be; given the reactions presented.

As these two findings are the only one's that came up in my search it appears that information on Anti A1 and it's clinical relevance is limited and conflicting. As such, I would still respectfully disagree with giving this patient A or AB rbc's because of the unnecessary additional, and potential, complications that may arise post transfusion and/or additional unnecessary complications with the Blood Bank work-up and compatibility testing. The article from the National Institute of Health suggested B rbc's as well as O rbc's. The B rbc suggestion seems better then O rbc's because the majority of B rbc donor would have residual Anti A1  for which the patient has been shown to not have the A1 antigen, and the patient (recipient) is also shown to not have Anti B; however this type may be limited in their inventory.

Do you or Malcom know of any other current articles addressing the clinical significance of Anti A1?

Thank you for any reply,

Ronald

 

 

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Hi Ronald,

I don't know of any current articles (by that, I take it you mean peer reviewed papers/posters/abstracts) concerning anti-A1, but I do know of three fairly recent books, written by world renowned authors, that say anti-A1 is only very rarely clinically significant, and not unless the antibody reacts at 37oC.  The probability is, as far as the rarity of recent articles on clinically significant anti-A1 is concerned is precisely because it is so rare.  The three books are:

Reid ME, Lomas-Francis C, Olsson ML.  The Blood Group Antigen FactsBook.  3rd edition, 2012, Academic Press, page 50.

Klein HG, Anstee DJ.  Mollison's Blood Transfusion in Clinical Medicine.  12th edition, 2014, Wiley Blackwell, page 419.

Daniels G.  Human Blood Groups.  3rd edition, 2013, Wiley Blackwell, page 53.

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Thank you Malcom and Galvania for providing these texts. I look forward to reading them. But, I would also like to ask you if there is anything written in these texts that states that there is a conclusive benefit for our 87 year old oncology patient, who appears to type as an A variant B, Rh Positive, and who tests negative for the A1 antigen, in acquiring an Anti A1 in addition to other considerable clinical variables?  Or is there any conclusive evidence of a definitive benefit in acquiring an Anti A1 for any other patient population?

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35 minutes ago, goodchild said:

I have to admit I'm confused Ronald. Why the focus on anti-A1? With the O or B blood that you suggest, would you also be prophylactically matching Rh, Kell, Duffy, Kidd, and MNS blood group system antigens?

This is the exact point I was making in my post of 30th December 2015 goodchild.  An anti-Jka, for example, is very clinically significant, but, as far as I can see Ronald, you are not suggesting that you would type your patient for the Kidd antigens and then, for example, if your patient is Jk(a-b+), give only Jk(a-) blood to your patient.  I might say, incidentally, that if you extrapolate this idea to all of your patients, your budget for blood would have to be enormous, and your blood supplier would very soon run out of suitably typed blood!  Incidentally, the Jka antigen is very much more immunogenic than is the A1 antigen.

I am not sure if your question, "Or is there any conclusive evidence of a definitive benefit in acquiring an anti-A1 for any other patient population?" is serious or not, but I will treat it as serious.

No, I know of no evidence, conclusive or otherwise, but were I an A2 individual, or an A2B individual (I'm an A1, as it happens), I would far rather produce an anti-A1, than an anti-S, an anti-s, an anti-K, an anti-Fya, an anti-Fyb, an anti-Jka or an anti-Jkb - all of which are seriously more clinically significant than an anti-A1, and, more to the point, was I to require a transfusion, even a top-up transfusion, and knowing what I know, even if I had an anti-A1, I would quite happily accept A1 or an A1B units of blood (A1B only if I were an A2B, of course, rather than an A2!!!!!!!!!!!!!!!!!!!!!!!).

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5 hours ago, Malcolm Needs said:

This is the exact point I was making in my post of 30th December 2015 goodchild.  An anti-Jka, for example, is very clinically significant, but, as far as I can see Ronald, you are not suggesting that you would type your patient for the Kidd antigens and then, for example, if your patient is Jk(a-b+), give only Jk(a-) blood to your patient.  I might say, incidentally, that if you extrapolate this idea to all of your patients, your budget for blood would have to be enormous, and your blood supplier would very soon run out of suitably typed blood!  Incidentally, the Jka antigen is very much more immunogenic than is the A1 antigen.

I am not sure if your question, "Or is there any conclusive evidence of a definitive benefit in acquiring an anti-A1 for any other patient population?" is serious or not, but I will treat it as serious.

No, I know of no evidence, conclusive or otherwise, but were I an A2 individual, or an A2B individual (I'm an A1, as it happens), I would far rather produce an anti-A1, than an anti-S, an anti-s, an anti-K, an anti-Fya, an anti-Fyb, an anti-Jka or an anti-Jkb - all of which are seriously more clinically significant than an anti-A1, and, more to the point, was I to require a transfusion, even a top-up transfusion, and knowing what I know, even if I had an anti-A1, I would quite happily accept A1 or an A1B units of blood (A1B only if I were an A2B, of course, rather than an A2!!!!!!!!!!!!!!!!!!!!!!!).

Malcom and Goodchild, as we all know there is already general risks of transfusion. Anti A1 does not have a great association with adverse effects of transfusion but there are rare cases as have been mentioned. This possibility is staring us right in the face from the work-up presented. So why not avoid by suggesting O rbc's or B rbc's? You know that there are more than enough times that we cannot avoid a conflict but this is not one of them at the moment. So, again I would ask, what is the benefit to our patient if they do acquire an Anti A1 that was completely avoidable?

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10 hours ago, Malcolm Needs said:

Ronald, It is obvious I am not going to convince you that this totally safe option goes on every day throughout the world, with no clinical sequelae, so I am no longer going to even try.

Malcom, I am not trying to be so strong headed hear to simply fight to win. There is really no winning or losing hear as some would suggest.

I know that when any blood bank product is transfused there is no first pass effect as when we take oral medication. If oral medication does not agree with you your digestive system will void it one way or another; and I think we may have all experienced this. But when a blood product is transfused it goes directly into the vein and there is no getting rid of it (at least not as quickly as the digestive system) and so knowing this I do not take any chances, slim or otherwise if I do not have to. And in this case we do not have to.

But let me explain another way. I am going to use the Chicken example and I am not trying to insult anyone's intelligence here. Suppose you go to your neighborhood market, that you frequent enough to know some of the staff and they know you. And so you go into the market and you go to the case where your favorite chicken brand is; and you look and pick a package of this chicken and go to place it in your cart when one of the market staff comes to you and says, Malcom I know that this is your favorite chicken brand but there was a problem at another location where this brand of chicken was implemented as being the cause of possible food poisoning do to Salmonella. Now only one news agency has done a story on this and you have not heard this news but you are hearing it from this market staff member who you know. Now, the staff member goes on to tell you that the shipment of chicken that was implemented went to another location but just for safety and because their investigation not complete, and there is a very slim chance that the package of chicken that you just put in your cart and will have for dinner along with your family maybe contaminated. It's the slimmest of chances and it's your favorite brand but it may be contaminated  and they will not know until their investigation is complete in a couple of weeks. Now there are a couple of other brands in the next case over of equal quality but not implemented as being the cause of this food poisoning. What would you do? Would you take the chance, slim as it may be, in contracting food poisoning or just simply pick another brand. Myself, I would pick another brand until the investigation is complete; and I am pretty sure that everyone else here would do the same.

It's just like this case. We do not have to take any chance because we have viable options. If we did not have these other options I would fully agree with you. But we have other options so why take even the slimmest of chances when we have the information that is given. An I know that there are always risks in transfusion as some of the other posters have mentioned, but this is a risk we are not forced to take; so why take it, as slim as it is?

Edited by rravkin@aol.com
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