PathLabTalk

Register now to gain access to all of our features. Once registered and logged in, you will be able to contribute to this site by submitting your own content or replying to existing content. You'll be able to customize your profile, receive reputation points as a reward for submitting content, while also communicating with other members via your own private inbox, plus much more!

This message will be removed once you have signed in.

Clarest

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

21 posts in this topic

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

 

Share this post


Link to post
Share on other sites


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.

rravkin@aol.com, yan xia and MOBB like this

Share this post


Link to post
Share on other sites

I think I am missing something.  When we identify an anti-A1 it is typically at immediate spin in the back type.  So wouldn't that mean that my immediate spin crossmatch with A or AB would not be compatible ?

BldBnker likes this

Share this post


Link to post
Share on other sites

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

Share this post


Link to post
Share on other sites

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

Malcolm Needs likes this

Share this post


Link to post
Share on other sites
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!!!!!!!!!!).

Share this post


Link to post
Share on other sites

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.

Share this post


Link to post
Share on other sites

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.

tkakin likes this

Share this post


Link to post
Share on other sites

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).

galvania likes this

Share this post


Link to post
Share on other sites
Quote
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!

Share this post


Link to post
Share on other sites

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

tkakin likes this

Share this post


Link to post
Share on other sites

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.

exlimey likes this

Share this post


Link to post
Share on other sites
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.

exlimey and Malcolm Needs like this

Share this post


Link to post
Share on other sites
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. 

Share this post


Link to post
Share on other sites

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. 

Share this post


Link to post
Share on other sites
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.

galvania and Veejay like this

Share this post


Link to post
Share on other sites

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.

Malcolm Needs likes this

Share this post


Link to post
Share on other sites
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.

Share this post


Link to post
Share on other sites
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!

 

Malcolm Needs likes this

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!


Register a new account

Sign in

Already have an account? Sign in here.


Sign In Now

  • Advertisement