Anti-Leb causing an acute transfusion reaction.

[Malcolm Needs ☆]

There is a short, but very interesting case report in Transfusion that may be of interest to members, especially those using solid phase technology.  It is:

 

Irani MS, Figueroa D, Savage G.  Acute hemolytic transfusion reaction due to anti-Le^b.  Transfusion 2015; 55: 2486-2488.

 

There are lessons to be learned, particularly the need to resolve ABO typing discrepancies prior to a transfusion.

 

I hope you enjoy it.

 

       

[galvania]

Any chance of posting the article, Malcolm?

Anna

[Malcolm Needs ☆]

Sorry Anna, but I'm not certain that I can, because of the strict copyright laws in the UK.

 

If I photocopied it, I can only use the photocopy for my own use.

 

It should be fairly easy to get hold of a copy (you can sometimes go to the Transfusion site on your computer, and it will let you see one paper in the present edition - you may be able to get it by that method?).

[Auntie-D]

The abstract can be found here

 

http://www.ncbi.nlm.nih.gov/pubmed/26018602

[Dr. Pepper]

Must be why those antibody activity charts say "usually" and "rarely" instead of "always" and "never".

 

Interesting article; thanks, Malcolm.

Edited October 22, 2015 by Dr. Pepper

[galvania]

Point taken Malcolm - I'll get it eventually - the journals do the rounds here and it can take a while!

 Thanks for the Abstract Dr. Pepper.

But now, this is an interesting one, because if it was not active at 37°C in IAT and only active in saline at RT, would anyone have considered it as being clinically significant?  Does the full article go into any more details, Malcolm?

[Malcolm Needs ☆]

To be honest, not a huge amount Anna, but the findings from the Reference Laboratory are convincing.

[galvania]

Do you know if this was just a solid screen thing?  Were other methods tested on the pre-transfusion sample and found positive?  I find this case really worrying.....

[galvania]

Me again - and if she was group O, you would not see it as an ABO discrepancy.

[Dr. Pepper]

They say it reacted at all phases with LISS, with PeG and gel methods and showed in vitro hemolysis by tube. The patient had received 2 Le(b+) units 9 days earlier, got a nice, expected bump in hgb, but was anemic again and was given the unit she had the reaction to. The backtype discrepancy was noticed before the last transfusion but chalked up to a cold agglutinin and not worked up. DATs were 1+ IgG, 2+ C3 before, 1+ IgG, 3+ C3 post-rxn. They report the antibody was IgM only with a titer of 256.

[galvania]

So it did come up in gel pre-transfusion in the IAT?  I totally get why they disregarded the discrepancy in the reverse. You get a discrepancy, and do a panel.  Pos at RT, neg in IAT and ??saline at 37°C.  You know that this is not clinically significant so you ignore it.  I can't say I would not have done the same.  In vitro haemolysis in tube - but presumably you would not have seen that either if you had EDTA plasma and EDTA in your cells.  And I really don't understand that there was NO reactivity at 37°C.  It must have had complement present to cause the haemolysis, and the AHG reagents mostly contain anti-C3d as well as anti-IgG, which anyway will cross-react mostly to some extent with IgA and IgM. 

Confused

[Dr. Pepper]

I think Malcolm's point was that they didn't do a panel when they noticed the typing discrepancy, but just assumed it was an insignificant cold because their solid phase screen was negative. Had they done a panel in tube or gel, they would have seen it, and probably seen a positive auto control, and done the DAT....I'm a little confused about the DAT - where did the IgG come from? Eluates were negative. They investigated a possible drug antibody but that didn't turn up anything.

[Malcolm Needs ☆]

You are correct about the points I was making Phil, but also they did try detecting the antibody by solid phase - and they couldn't!

[Dr. Pepper]

Anna pointed out that they wouldn't have had a hint of the antibody had the patient been group O. So this then becomes an acceptable risk of transfusion, like the 1 in 10,000 incompatibility that would have been caught by a full crossmatch but missed by IS or electronic when the patient has an antibody to an antigen not on the screening cells. It's interesting what we consider acceptable or not. Our industry spends a lot of money shaving very small slices off of very small piles of risk - like WNV testing, for example. But we accept other risks, like the above, or possible hemolysis from minor side incompatbile platelets and so on. 

[Malcolm Needs ☆]

I agree, but it would cost an awful lot more going back to clotted samples, as we then couldn't group them by automation.