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Questions about a potential A subgroup


AmyL86

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14 minutes ago, Malcolm Needs said:

So, you would give your patient WASHED group O or A2 units of blood, in case there is a minute chance that the small amount of plasma contained in a unit of packed cells is high titre and may destroy some of the recipient's own red cells?

Sorry, but as I posted above, that's it on this thread from me.

I have to believe that this is an elaborate trolling event.

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15 hours ago, Malcolm Needs said:

So, you would give your patient WASHED group O or A2 units of blood, in case there is a minute chance that the small amount of plasma contained in a unit of packed cells is high titre and may destroy some of the recipient's own red cells?

Sorry, but as I posted above, that's it on this thread from me.

Malcom, you are right. We do not have to be concerned with Anti A1 because we will cross match units of B Pos rbc's and O Pos rbc's as needed because this patient tests like an Avarient B, Rh Pos, A1 antigen negative, and therefore we can give B Pos or O Pos rbc's as the patient's results depict. We only need to be concerned with Anti A1 is if we attempt to transfuse A or AB rbc's and cause the potential production of Anti A1 which has not been shown to offer any benefit for the patient along with all other antibodies. As a matter of fact how do we know that if the patient is sensitized to the A1 antigen that this will not trigger further sensitizations to other far more clinically impacting antigens. You know about this possibility with other patient populations requiring continued therapeutic transfusions. So all I am saying is avoid the whole mess of possibilities, rare as they may be, and give B Pos or O Pos rbc's; because in this case we can. Let me further ask you how is it that one of these very rare detrimental events comes to be known and recorded; of course, during or after the transfusion. If you look at the number of cases of ABO transfusion reactions within the previous ten years you will see miniscule numbers. ABO incompatibility is also an extremely rare event. But the organizations that govern practice in our field have the goal to prevent any transfusion reactions despite the miniscule number of occurrence. This is a responsibility that they take on as governing bodies within our practice. We have the same responsibility, so when we have the opportunity to avoid a non-beneficial antibody production we are responsible to take that opportunity when it presents itself; because you know that we do not always have this opportunity. So save your facts and extensive information for the times that we do not have the opportunity and be responsible in either case.

So why do we need to be responsible? Because sick patients are at varying levels of vulnerability. For instance, our patient here is hospitalize and receiving apparent therapeutic transfusions. This patient is vulnerable to all of the benefits and liabilities of each level care they receive. If this patient would lose consciousness then they are at an extreme level of vulnerability comparable with that of an infant. We wouldn't take unnecessary and non-beneficial risks with an infant, would we? No, because we are responsible; and we are human.     

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I would consider myself to be extremely responsible. I have had 40 years + working in the field to learn that responsibility. And I also have enough experience in blood transfusion to know when something is a risk and when it isn't, and when I don't know . And I don't think Malcolm will mind if I say that so is he responsible and he has even more experience and much more knowledge than me.  People like Marion Ried, Geoff Daniels and Issitt who we quoted before have even more.  All these people state that anti-A1 is NOT a risk.  I am sure that you are not saying tha you are more responsible than all of these people.  I don't know how else I can put this so you stop thinking of anti-A1 as a risky antibody and spend your time and energy trying to prevent the ones that are!.

 

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44 minutes ago, galvania said:

I would consider myself to be extremely responsible. I have had 40 years + working in the field to learn that responsibility. And I also have enough experience in blood transfusion to know when something is a risk and when it isn't, and when I don't know . And I don't think Malcolm will mind if I say that so is he responsible and he has even more experience and much more knowledge than me.  People like Marion Ried, Geoff Daniels and Issitt who we quoted before have even more.  All these people state that anti-A1 is NOT a risk.  I am sure that you are not saying tha you are more responsible than all of these people.  I don't know how else I can put this so you stop thinking of anti-A1 as a risky antibody and spend your time and energy trying to prevent the ones that are!.

 

Galvania, I was brought up in blood bank to not only rule out possible compatibility issues as far as the presence of antibodies is concerned but to also not provoke a possible antibody, no matter how clinically significant. All I was trying to say is that I disagree with this recommendation because it directly conflicts with my training and experience; and if the production of an antibody is none beneficial and avoidable why is this such a problematic course of action?  I know that you and Malcom know a world about blood bank and I definitely respect that, and if I can only learn and know a fraction of what you both know I would definitely feel some level of accomplishment. But in any relationship there are naturally going to be disagreements. We share the same passion. So how can we disagree in the future?

Edited by rravkin@aol.com
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Quote

I was brought up in blood bank to not only rule out possible compatibility issues as far as the presence of antibodies is concerned but to also not provoke a possible antibody, no matter how clinically significant

It just seems like if that is your argument, then you should be giving phenotypically matched units to all your patients. I do not see the difference from the position you seem to be making.

Edited by Teristella
Adding quote.
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2 hours ago, Teristella said:

It just seems like if that is your argument, then you should be giving phenotypically matched units to all your patients. I do not see the difference from the position you seem to be making.

Teristella, I have not made my argument clear. The practice is that we do not provoke potential antibody production if we can avoid it. When there is no clincal benefit for the patient from producing an antibody and it is completely avoidable based on their type and screen we should avoid it. I keep seeing this same argument about how we should just go ahead and give phenotypically matched units, but this is not what I am saying. So I will repeat, what I am saying is that if we know of an apparent possibility for our patient to acquire an antibody(s) based on the type and screen results, and it is avoidable then we should avoid it. If the patient demonstrates an Anti M or had a history of it, which is also apparently not but so clinically significant, would you not phenotype the donor for Anti M If you carry the antisera, or would you at least perform an extended crossmatch; or would you say "It's not clinically significant in the majority of cases, therefore we do not have to be concerned if the patient acquires this antibody." Please let me know if this is clear.

What Malcom and others are suggesting here is that it is OK to give AB Pos red cells to this patient who types as an apparent A variant B, Rh Pos and that despite the fact that the majority of AB donors are actually A1B then there is a distinct possibility that this patient with develop an Anti A1; which everyone has said in some way or another that it is not a clinically significant antibody. However, there are noted rare cases when this antibody is found to be clinically significant and there is not a whole lot of information out about Anti A1. But can and anyone here tell of what clinical benefit this 87 year old Oncology patient can expect to receive from potentially acquiring an Anti A1? I have spoken about this patient's immuncompetancy  and I realize that he may not even be capable of producing and antibody base on has age clinical condition. But we can avoid any possibility of any rare event here, with this case, because we know that this patient is an A variant B; so all we simply have to do is provide this patient with compatible O red cells or B red cells, for which the pathologist involved has done.  

To further elaborate on these comments of " why don't we just give phenotypically matched red cells to everyone," in some cases we already do. For instance a patient that requires frequent therapeutic transfusions; as most of you know, many blood banks practice to give Rh and Kell match red cells in order to avoid the well enough documented chain of sensitizations that occur starting with Rh antigens and proceeding through to Kell, Duffy, Kidd, etc. I am not trying to suggest this here, but for those who cling to this argument look around, because I firmly believe that this is where we are headed once the cost is contained; and this quest is fueled by the agencies that govern blood bank practice and businesses who will profit from this practice.   

In closing, I am a practicing bench Technologist who does not have the degree of expertise as Malcom and others, but I firmly believe that if acquiring an antibody is not beneficial for the patient and it is completely avoidable without any extra exertions then we should avoid it. Let me leave you with this question, How many times have you encountered a case where you didn't have a choice but to run the risk of antibody(s) development in your recipient? Did it make you nervous? Did it make you nervous such that after you investigated the potential antibody and found that it was clinically insignificant you were relieved. Then you are understand what I am saying here because your first instinct was to avoid the production of this antibody in the first place because somewhere in your practice you learned and saw through experience that antibody production was something to be avoided, as we all have,  and over years of practice this instinct becomes second nature. :)

Edited by rravkin@aol.com
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Ronald - you do know, don't you, that the anti-A1 antibodies that are found in A2 people are 'naturally occurring' or non-red-cell immune?

Facts:

1.  All individuals have a greater or lesser potential of making antibodies against all antigens they come in contact with that they themselves do not possess when they are either transfused or pregnant.

2.  You can never transfuse (or choose your husband) with blood that exactly matches the patient that needs transfusion.

3.  Over the years, as experience has grown, experts have made decisions about which antigens are immunogenic, which antibodies are dangerous, and consequently, what it is necessary to avoid and what needs to be taken into consideration at all times, most of the time, except in an emergency.  For example, exposure to a D antigen needs to be avoided in 'young' women except in a dire emergency, but can be given to men in some circumstances.  A person with an anti-Jka once found should always be given blood that has been phenotyped as Jka-.  Anti-A1 does not have to be taken into consideration (and the avoidance of producing an anti-A1 does not have to be taken into consideration) except in the EXTREMELY rare cases where the anti-A1 is active at STRICTLY 37°C.  That is the state of knowledge now.  40 years ago when I started we had less experience and less knowledge and we were more worried about antibodies that are now known not to be clinically significant.  But things have moved on since then.  Thank goodness!

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57 minutes ago, galvania said:

Ronald - you do know, don't you, that the anti-A1 antibodies that are found in A2 people are 'naturally occurring' or non-red-cell immune?

Facts:

1.  All individuals have a greater or lesser potential of making antibodies against all antigens they come in contact with that they themselves do not possess when they are either transfused or pregnant.

2.  You can never transfuse (or choose your husband) with blood that exactly matches the patient that needs transfusion.

3.  Over the years, as experience has grown, experts have made decisions about which antigens are immunogenic, which antibodies are dangerous, and consequently, what it is necessary to avoid and what needs to be taken into consideration at all times, most of the time, except in an emergency.  For example, exposure to a D antigen needs to be avoided in 'young' women except in a dire emergency, but can be given to men in some circumstances.  A person with an anti-Jka once found should always be given blood that has been phenotyped as Jka-.  Anti-A1 does not have to be taken into consideration (and the avoidance of producing an anti-A1 does not have to be taken into consideration) except in the EXTREMELY rare cases where the anti-A1 is active at STRICTLY 37°C.  That is the state of knowledge now.  40 years ago when I started we had less experience and less knowledge and we were more worried about antibodies that are now known not to be clinically significant.  But things have moved on since then.  Thank goodness!

Hi Galvania, congratulations, you and I were writing our posts here at exactly the same time. I did not know that Anti A1 antibodies were naturally occurring in A2 patients but I understand why, in that they follow the same course of development as the other ABO antibodies and it makes sense. I am under the impression that your Fact #1 is also applicable to Anti A1 as well. However if anti A1 is acquired this way it, in most cases will remain an IgM class antibody ( like the other ABO antibodies are) but in rare cases they can seroconvert to IgG were they can become more clinically significant; as with an A type mother who delivers a B type infant; any Anti A antibodies that made their across the placenta are definitely IgG.

Your fact number 2# is a little confusing in that I thought that women in the majority of the world were able to choose their husbands and few cultures still practice otherwise; And why would you want to right away transfuse your husband, don't you think watching a movie and maybe some dinner first is more interesting. ( I am sorry but I couldn't resist.) I am aware of the rarity of exact match as I have worked in tissue typing lab where crossmatches are virtually never fully compatible.

And lastly Fact#3, I am aware of what you are saying here and when pressed, discussions based on the clinical significance of an antibody are made. However, a differing in practice here with anti A1; as you state ".. in ETREMELY rare cases where anti-A1 is active STRICTLY at 37C," when we have the opportunity to remove the possible of this extremely rare event we should take it as part of our practice in blood bank. As I believe I asked before, When is a rare event documented?; during or after the transfusion. If you have a case where you are deciding between a potential for Anti A1 and a Kell and this is unavoidable, well it's obvious to run the risk of acquiring an Anti A1 as opposed to the Kell. But here we do not even have to consider Anti A1 and it's rare potential or otherwise; just give O Pos or B Pos red cells. But let me ask you this, Is there any less benefit for this patient in receiving O Pos or B Pos red cells? Is it  more beneficial to transfuse AB red cells?

I also want to thank you for taking out the time to write this post; I do greatly appreciate it.:)

Edited by rravkin@aol.com
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3 hours ago, goodchild said:

Considering that in the grand scheme of things, blood inventory management is a community responsibility, using group O blood for this patient would be seen by the vast majority of blood bankers as harmful/wasteful.

Goodchild, when is the last time you ran out of group O Rh Pos red cells as compared to AB Pos red cells? And what about group B Rh Pos red cells? Does your blood bank reside in area where AB Rh Pos red cells is the predominant type and types O and B are scarce? If so then, by all means, give AB Rh Pos red cells; and does your blood bank have electricity and running water?

                Sight in the absence of light leaves you blind.:rolleyes:

Edited by rravkin@aol.com
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Dear Ronald

I think your reply to Goodchild is a little out of order!

Your comments about what I said about women chosing their husbands made me laugh.  I was of course referring to choosing one's husband according to their blood group - which becomes relevant during pregnancy - mostly not their ABO group, certainly not their A sub-group (anti-A1 has NEVER caused HDN), but things like Rh antibodies.

And the point about not wasting group O blood on non-O patients is this.  Group O patients can ONLY receive group O blood.  Group AB patients can have AB, A, B or O.  So, if you don't have group AB blood in stock you can give group A (and I insist, you do NOT have to type to make sure the blood is A2B), or B; if you're in Europe or America you're more likely to have more group A than B so you can give B.  If you run out of A blood in an emergency you can give your group A patient group O.  If you run out of group O blood, and you have a group O emergency you are well and truly stuck.

I am going to say again - anti-A1 does not constitute a risk for the patient.  Anti-A1 is a weak antibody that reacts in the cold.  As I said above, it is a naturally occurring antibody.  Naturally occurring antibodies do not switch in the same way as 'proper' antibodies.  Anti-A and anti-B are exceptions.  There is absolutely no comparison between anti-A and anti-A1.  It's like comparing Mount Everest to an ant-hill.You can transfuse an A2 patient who already has a 'normal' anti-A1 with A1 blood - and nothing will happen.  If you try transfusing a Jka- patient with an anti-Jka with Jka+ blood - then you'll be in big trouble.

The chances of your stimulating the production of an anti-A1 in an A2 patient through transfusion when they haven't already made a naturally occurring one is infitesimally small.  The chances of stimulating the production of an antibody against another red cell antigen (Kidd, Duffy, Ss) for example are considerably larger; against Rh antibodies much larger again; and D is the Mount Everest of the story.  And yet we do not, apart from D, and except in very specific cases, worry about preventing antibody stimulation against these antibodies.

Please, Ronald, stop worrying about anti-A1.  Do you give Rh and K matched blood to all your women needing transfusion?  If not, start worrying about that.  Do you give Rh, Kell and Duffy matched blood to all your sickle cell patients.  If not, start worrying about that - big time.

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My view is that the OP clearly doesn't understand transfusion science.

The worst that is going to happen is they might develop a clinical insignificant antibody - so what? So what if it is even clinical significant? If they ever come in needing blood again - then  you worry about giving antigen negative blood. Hell - I've given O+ blood to an O- WOMAN of CHILD BEARING AGE in a massive haemorrhage situation. And do you know what? She didn't develop an anti-D!

The patient is group B - exactly how many units do you think you will have access to that are antigen negative for every antibody the patient has any possibility of developing? You are going to severely limit your donor pool.

The patient in question may not ever need a transfusion again - you are worrying about a miniscule maybe.

I seriously think you are overthinking this but not actually grasping the concept.

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16 hours ago, rravkin@aol.com said:

Goodchild, when is the last time you ran out of group O Rh Pos red cells as compared to AB Pos red cells? And what about group B Rh Pos red cells? Does your blood bank reside in area where AB Rh Pos red cells is the predominant type and types O and B are scarce? If so then, by all means, give AB Rh Pos red cells; and does your blood bank have electricity and running water?

                Sight in the absence of light leaves you blind.:rolleyes:

You are aware that if you run out of B or AB units it is perfectly acceptable to give group O? You are competent enough to know that?

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