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Transfusion for a group A2B with anti-A1 sickle cell disease patient


Clarest

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Hi all,

If a sickle cell disease patient is group A2B with anti-A1 (seems no reactivity at 37 degree), which ABO group of donor cells is the best choice for transfusion, group O or B immediate-spin crossmatch compatible, or group A IAT crossmatch compatible? Thank you for your reply.

Clarest

 

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6 hours ago, Clarest said:

Thank you Malcolm. We do not usually keep group AB red cell units in our stock.

Yes, there are some hospitals in the UK that do not keep group AB red cells.  The original excuse/reason was that they did not have that many group AB patients, and so the units expired.  As a result, group AB units were, essentially, made "free", in that, if they were not used, the cost was refunded.  Still some hospitals did not want to stock them and, privately, I was told this was because they were frightened that they would be given in error to a group A, B or O patient (which is a huge worry, if they think that they and their staff cannot perform accurate ABO typing on patients).

In your case, it is different, as you know that you have a "tame" group AB patient who will be, presumably, be using the blood on a regular basis.  If you still don't want to transfused group AB blood, I would go for A first, as the anti-B in those units tend to be of lower titre and avidity than does the anti-A in either group B or O units, but, in my opinion, it would be better to give AB red cells.  There was a paper recently, I think in Transfusion, but I'm not certain (and I am just about to rush out for an appointment, so I can't check now) that highlighted the fact that ABO antibodies can cause clinical problems other than haemolytic transfusion reactions.

Sorry this was written in such great haste.

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Hi Malcolm,

We gave group A IAT crossmatch at first when  group AB was not available in our stock. Then,  we particularly ordered group AB units to hold for this patient. I am really interested in the paper you mentioned in your post regarding AB antibodies. When you have time, could you please share it with us?

Thanks a lot. 

Clarest

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Hi tkakin,

You're right that anti-A1 typically reacts at immediate spin and that's reason for us to give group A or AB IAT crossmatch compatible red cells. On the other hand, if the group A or AB units are IAT crossmatch compatible with patient's plasma, it  proves the anti-A1 does not react at 37C.

Clarest

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5 hours ago, Clarest said:

 

5 hours ago, Clarest said:

I am really interested in the paper you mentioned in your post regarding AB antibodies. When you have time, could you please share it with us?

Thanks a lot. 

I will do my very best to look it up over the weekend (between international rugby matches on the television!!!!!!!!!!).

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Well, you can't rely on my memory - it wasn't Transfusion at all, but Vox Sanguinis!  The reference is as follows:

Zaffuto BJ, Conley GW, Connolly GC, Henrichs KF, Francis CW, Heal JM, Blumberg N, Refaai MA.  ABO-immune complex formation and impact on platelet function, red cell structural integrity and haemostasis: an in vitro model of ABO non-identical transfusion.  Vox Sanguinis 2016; 110 (3): 219-26.

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If you use Ortho gel for your IAT XMs they say that you must also do some other method to detect ABO incompatibility as their gel can't be relied upon to detect it.  So you can't skirt the incompatibility by doing just an IAT XM (unless you have an alternate approach to determining the ABO compatibility of the unit that is unaffected by the anti-A1). Our computer system would get all antsy about us giving A units unless they were specifically A2.  We just give O to keep the computer happy and make life easier.  Dr. Blumberg has been trying for years to get people to pay attention to the risks immune complexes.  Maybe I should read that paper.

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I DO understand the business of a method to detect ABO incompatibility Mabel, BUT, if you have a known group A or AB patient with an anti-A1 that, in addition has been shown NOT to be reactive at 37oC, there must, surely, be a way around it?  What do you do, for example, if the patient has cold haemagglutination disease, with a high titre, very avid auto-anti-I?  Surely, the same must apply, that all units will be apparently ABO incompatible by normal immediate spin techniques?

In addition, surely your computer programme should be written so that it helps you, rather than hinders you?  It seems to me that, if the human being knows that group A blood, whether it be A1, A2 or any other subgroup of A, will be efficacious for the patient, the computer programme should not prevent the human being from giving that blood, and that the computer programme needs to be rewritten as a matter of urgency.  This is particularly important to prevent the wastage of finite group O red cells, but more particularly, if the in vitro findings of Zaffuto et al are found to extend to the in vivo situation (or even if there is the slightest suggestion that they so do).

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On 6/17/2017 at 11:40 AM, Malcolm Needs said:

Well, you can't rely on my memory - it wasn't Transfusion at all, but Vox Sanguinis!  The reference is as follows:

Zaffuto BJ, Conley GW, Connolly GC, Henrichs KF, Francis CW, Heal JM, Blumberg N, Refaai MA.  ABO-immune complex formation and impact on platelet function, red cell structural integrity and haemostasis: an in vitro model of ABO non-identical transfusion.  Vox Sanguinis 2016; 110 (3): 219-26.

 

Thanks a lot Malcolm!

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Hi Mabel,

We use the tube saline IAT method for crossmatch and it is allowed to skip the immediate-spin phase. So, as long as the anti-A1 does not react at 37C, we have no problem to result the compatibility of the crossmatch. Routinely, it is okay for us to give group O or B  blood for patient's with anti-A1 and that's what technologists prefer to do as it only requires immediate spin. However, for this particular patient, we just wanted to be more careful. 

Clarest

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On ‎6‎/‎18‎/‎2017 at 2:52 AM, Malcolm Needs said:

In addition, surely your computer programme should be written so that it helps you, rather than hinders you?  It seems to me that, if the human being knows that group A blood, whether it be A1, A2 or any other subgroup of A, will be efficacious for the patient, the computer programme should not prevent the human being from giving that blood, and that the computer programme needs to be rewritten as a matter of urgency.  This is particularly important to prevent the wastage of finite group O red cells, but more particularly, if the in vitro findings of Zaffuto et al are found to extend to the in vivo situation (or even if there is the slightest suggestion that they so do).

In Meditech, user can designate whether an antibody is/is not clinically significant and can also designate corresponding antigen-negatives.  In the case of anti-A1,  you could create two 'anti-A1' entries in the 'antibody file'.  One would be designated "clinically-significant' and that A2 cells were 'antigen-negative'.  The second entry in the antibody file would not be designated 'clinically-significant' and the 'antigen-negative' field left blank.  For patients with an anti-A1 that reacts as 37C, computer would require A2 red cells for crossmatch.  Patients with anti-A1 that does not react at 37C would not require A2 cells.

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On 6/19/2017 at 11:38 AM, BldBnker said:

Why couldn't you give B blood (packed cells)?  The Anti-A1 would be avoided and the blood would be compatible.  AB is the "universal receiver" after all.  Just curious.

As Malcolm mentioned " as the anti-B in those units tend to be of lower titre and avidity than does the anti-A in either group B or O units". The patient is group AB and the red blood cells have A and B antigens. 

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I would worry more about the Anti-A1 antibody than the low amount of Anti-A in the residual plasma of a B unit of packed cells.  If the Anti-A1 is present at immediate spin, then it is probably IgM just like Anti-A and Anti-B that are naturally occurring (which cause HTR).  We see these individuals occasionally and transfuse them with O blood (if it is an A subgroup with Anti-A1 antibody) and with B blood if its an A subgroup B individual with  Anti-A1.  The transfusions are successful.  I worry more about having to give type incompatible platelets that have way more plasma than a unit of packed cells. 

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1 hour ago, BldBnker said:

I would worry more about the Anti-A1 antibody than the low amount of Anti-A in the residual plasma of a B unit of packed cells.  If the Anti-A1 is present at immediate spin, then it is probably IgM just like Anti-A and Anti-B that are naturally occurring (which cause HTR).  We see these individuals occasionally and transfuse them with O blood (if it is an A subgroup with Anti-A1 antibody) and with B blood if its an A subgroup B individual with  Anti-A1.  The transfusions are successful.  I worry more about having to give type incompatible platelets that have way more plasma than a unit of packed cells. 

I am sorry BldBnker, but I, amongst others, thoroughly disagree with you about the clinical significance of anti-A1.  You must do what you feel safe to do, but I fundamentally disagree.  If you look at Marion Reid, Christine Lomas-Francis and Martin Olsson's book, The Blood Group Antigen FactsBook.  3rd edition, 2012, Academic Press, anti-A1 causes either no, or mild/delayed haemolytic transfusion reactions.  Their findings are backed up by Geoff Daniels in his book Human Blood Groups.. 3rd Edition, 2013 Wiley-Blackwell, Geoff Daniels and Imelda Bromilow in their book Essential Guide to Blood Groups..  3rd Edition.  2014, Wiley-Blackwell, Robina Qureshi in her book Introduction to Transfusion Science Practice.  6th Edition.  2015, British Blood Transfusion Society and Harvey Klein and Dave Anstee in their book Mollison’s Blood Transfusion in Clinical Medicine.  12th Edition, 2014, Wiley-Blackwell.  In other words, most of the world's leading blood group serologists and blood transfusion doctors disagree.

You are perfectly correct when you say that the anti-A1 detected by immediate spin is probably IgM, but, if you look at the findings of haemovigilance organisations throughout the world, most adults have an element of IgG (and IgA come to that) ABO immunoglobulins, and this is particularly so in the case of group O individuals, and, within that cohort, group O females who have been pregnant with an ABO-incompatible foetus.  It is these IgG antibodies, in conjunction with the ABO IgM antibodies that cause the worst (often fatal) transfusion reactions, but it is actually the effect of complement that makes these antibodies so clinically significant.

In addition, if you perform titration studies on anti-A and anti-B (and anti-A,B), the titres are almost always much higher than the titre of anti-A1, and this, again, influences clinical significance (human-derived high titre anti-A1 is as rare as hen's teeth).  The anti-A and/or anti-B in the small amount of plasma left on units that are not ABO identical to the recipient are, therefore, much more likely to cause a transfusion reaction (graft versus host) than is any anti-A1 (host versus graft).

Sorry to go on for so long.

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I just have a hard time transfusing red cells that yield a 1-2+ positive reaction at immediate spin (can't call that compatible  :o)  ).  That being said, we do what our pathologist requires.  I agree that O mothers delivering incompatible type babies have destructive IgG ABO antibodies.  We still do Lui Freeze Elutions on all neonates with positive DAT's to identify the "culprit" antibody.  I'm not sure many facilities continue to do that.

Thanks for the references.

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8 minutes ago, BldBnker said:

I agree that O mothers delivering incompatible type babies have destructive IgG ABO antibodies.

Not only that, but they are amongst the few IgG antibodies that cause agglutination of "normal" red cells without a potentiater (never sure how to spell that - and spelling is my bogey subject anyway!), but also do so at 4oC, through to the warm.

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3 hours ago, BldBnker said:

I just have a hard time transfusing red cells that yield a 1-2+ positive reaction at immediate spin (can't call that compatible  :o)  ).  ...

Let me spin this differently.  I'm unlikely to detect an anti-A1 or any other weakly reactive (1-2+) IgM antibody in routine room-temperature gel testing.  Secondly, I have eliminated the immediate-spin crossmatch in favor of an electronic crossmatch to detect ABO incompatibility between donor and recipient. Lastly, by adopting the electronic crossmatch, I have accepted that any reactivity (limited to room-temperature) between donor and recipient (not demonstrated to be due to anti-A and/or anti-B) is rendered clinically irrelevant!

 

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On 18/06/2017 at 4:01 AM, Mabel Adams said:

If you use Ortho gel for your IAT XMs they say that you must also do some other method to detect ABO incompatibility as their gel can't be relied upon to detect it.  So you can't skirt the incompatibility by doing just an IAT XM (unless you have an alternate approach to determining the ABO compatibility of the unit that is unaffected by the anti-A1). Our computer system would get all antsy about us giving A units unless they were specifically A2.  We just give O to keep the computer happy and make life easier.  Dr. Blumberg has been trying for years to get people to pay attention to the risks immune complexes.  Maybe I should read that paper.

Hi Mabel,

I am just setting a Journal Based Learning exercise for the Institute (I can't say the paper I'm using on here yet, as some of the members will be taking the exercise, and I shouldn't really give them any hints in advance of those who are not members on here), but I came across this statement,

"Accumulating data indicate that the infusion of plasma which contains ABO antibodies may cause the rapid clearance of platelets, formation of immune complexes, endo thelial cell damage and multiple organ dysfunction.", and the authors of the paper give the following references:

Heal JM, Blumberg N, Masel D.  An evaluation of crossmatching, HLA, and ABO matching for platelet transfusions to refactory patients.  Blood 1987; 70: 23-30.

Benjamin RJ, Antin JH.  AB)-incompatible bone marrow transplantation: the transfusion of incompatible plasma may exacerbate regimen-related toxicity.  Transfusion 1999; 39: 1273-1274.

Lapierre V, Mahe C, Auperin A, Stambouli F, Oubouzar N, Tramalloni D, Benhamou E, Tiberghien P, Hartmann O.  Platelet transfusion containing ABO-incompatible plasma and hepatic veno-occlusive disease after hematopoietic transplantation in young children.   Transplantation 2005; 80: 314-319.

I have not read these cited papers myself, but the authors of the paper I am using for the exercise must know what they are doing, as they also cite a paper written by some bloke named Needs!!!!!!!!!!

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On 6/19/2017 at 1:54 PM, Dansket said:

In the case of anti-A1,  you could create two 'anti-A1' entries in the 'antibody file'.  One would be designated "clinically-significant' and that A2 cells were 'antigen-negative'.  The second entry in the antibody file would not be designated 'clinically-significant' and the 'antigen-negative' field left blank.

Just like for an anti-M that either did or did not react at 37.

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  • 2 weeks later...

In general we do our best to not detect antibodies that do not react at 37 degrees and IAT, but obviously reverse grouping is performed at room temperature, so you are occasionally going to find an anti-A1.  We would probably not ignore this, despite the evidence that clinically evident hemolysis is very unlikely to nil.  Our approach would probably be washed group O red cells.  The reasoning is to minimize the infusion of incompatible soluble antigen and antibody from the ABO blood group.  It may well be overkill in this setting, but we are now convinced that the use of so-called universal donor group O red cells and group AB plasma is likely harming some patients by increasing bleeding, multi-organ failure and infection through an immune complex/hemolysis mechanism. 

Traditionally, hematologists and transfusion professionals are only worried about massive hemolysis.  Recent work by many groups suggests that low levels of hemolysis (say 10-50 mg/dl) are not benign. Free hemoglobin, heme and iron are clearly not benign in animal models.  We know from experiments of nature such as sickle cell anemia and paroxysmal noctural hemoglobinuria that these sorts of "invisible" levels of hemolysis likely cause vasculopathy, platelet activation and thrombosis and predispose to nosocomial infection.  Hence we are trying to never give transfusions that may contribute to hemolysis by infusing incompatible ABO antibody or soluble/cellular antigen.  Hence the saline washing of group O red cells in some instances in order to avoid both antibody as well as antigen incompatibility.  We have randomized trial data that this approach is safe (no excess bleeding) and reduces inflammation in cardiac surgery and improves survival in acute myeloid leukemia.  Moreover use of ABO identical and washed (and leukoreduced) transfusions almost completely abrogates the last platelet refractoriness seen in patients with hematologic malignancy.  Yes it's extra work and costs a bit more, but HLA matched platelets are expensive too :).

Finally, since converting to this policy of ABO identical everything for all recipients we have seen our febrile and allergic transfusion rates decrease substantially, and our red cell alloimmunization rates to CcEe and K have decreased by 50% or so.  We consider this good news.

 

One reason patients with sickle cell anemia have such high alloimmunization rates, we suspect, is the tendency to use group O red cells (unwashed) which creates low levels of ABO immune complexes in non-O recipients that predispose to immune activation.  No data on this, just suspicion and extrapolation from our clinical data.

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