I'll get back to you on this one Rashmi, BUT, it is the first day of the Six Nations today, so it will certainly not be until those matches are over!

I haven't forgotten my promise Rashmi, but I have been right up to my neck in work over the past few days.

Right then Rashmi, at long last I've got time to answer.

The answer to your first point is "NO". Part of the diagnosis of hyperhaemolysis (which is largely a diagnosis of exclusion, rather than inclusion) is that the post-transfusion Hb is ALWAYS lower than the pre-transfusion Hb.

The answer to your second question is also "NO". There is an increasing body of documentation that suggests that hyperhaemolysis is caused by hyperactive macrophages.

The patient to which you refer, as far as I know, has fulminating AIHA (remember, a negative DAT does NOT rule out AIHA). He did indeed have an anti-S-like specificity that was detected with papain-treated red cells only, and the reason we tried U- units was because, according to some work published by Jill Storrey a few years ago, this particular specificity is often an auto-anti-U that reacts preferentially with either S+ red cells or s+ red cells.

In this case it wasn't, because U- red cells, together with all the panel cells, reacted with the elution (unless, of course, the auto-antibody detected in the eluate had an Rh specificity that was also on the U- red cells.

I must admit that I am a bit surprised that he wasn't already on IVIG.

Thanks for your info Malcolm, IVIg seems to have helped.

Mechanical damage ruled out?  Transfusion process not suspect in any way?  Infusing with saline only?  Not likely thermal damage to units since it happens repeatedly. IgA, IgE or some other class of antibody? Do any others fix complement so as to cause intravascular destruction? I remember someone telling me once of an anti-E that killed a patient that they couldn't get to come up in any testing except, I think, enzyme. (Now that I think of it I wonder if what they found was an innocuous enzyme-only anti-E that was a red herring.)   What about one of those complement-dependent Kidd antibodies we always worry about but which are pretty rare?  The serum specimen should help but use poly AHG (or anti-complement anyway).  If the blood warmer keeps working, keep using it.  

 

Mechanical damage ruled out?  Transfusion process not suspect in any way?  Infusing with saline only?  Not likely thermal damage to units since it happens repeatedly. IgA, IgE or some other class of antibody? Do any others fix complement so as to cause intravascular destruction? I remember someone telling me once of an anti-E that killed a patient that they couldn't get to come up in any testing except, I think, enzyme. (Now that I think of it I wonder if what they found was an innocuous enzyme-only anti-E that was a red herring.)   What about one of those complement-dependent Kidd antibodies we always worry about but which are pretty rare?  The serum specimen should help but use poly AHG (or anti-complement anyway).  If the blood warmer keeps working, keep using it.  

 

Hi Mabel,

 

IgA can activate complement via the properdin or alternative complement pathway.  JoAnn Moulds reminded us of this at the "Who DAT" session at the 2013 AABB meeting in Denver last October. 

 

At this session Patricia Arndt spoke about negative DATs in patients with clinical hemolysis.  Patricia Arndt mentioned more sensitive methods that can demonstrate antibody on RBCs in these patients.  These methods include cold LISS wash DAT method, flow cytometry, direct Polybrene test, also testing with anti-IgA and anti-IgM reagents.  Anti-IgA and anti-IgM reagents are not commercially available in the US, but Pat's lab has these reagents for research and special cases. 

 

But Pat also mentioned that anti-IgG reagents that are not heavy-chain specific can pick up IgA and IgM because these reagents may have antibodies to kappa and lambda light chains and can react with IgA and IgM light chains.

 

Pat presented a case of a 5 year old with clinical hemolysis (Hgb = 6.4, bilirubin high, LDH high, etc) and a negative DAT.  It turned out this 5 year old had IgA on his RBCs which was detected using anti-IgA reagent, but an anti-IgG reagent that was not heavy chain specific also detected the IgA on the cells (weakly).  The cold LISS wash DAT and the Polybrene agglutination did not demonstrate the antibody in this particular case.

 

The 5 year old was treated with steroids.

 

Catherine

EXCELLENT post Catherine. Thank you.

And, Malcolm, Catherine just passed the SBB exam 4 months ago.  Pretty smart cookie, isn't she?

She most certainly is Mabel. Congratulations Catherine.

Jsut returned from a break (watching Oz beat Engl in cricket 5 - zip {Sorry Malcolm}) to see a most interesting discussion. I remember something similar many moons ago in a cancer patient, but can't add specifics. That aside I would be most interested to hear if there is a resolution to this case Laurie.

Despite being bad for the patient, this is very interesting to all BBers as who knows when it could crop up in our hospital/s.

 

Cheers

Eoin (Wayne E)

You are not in the least sorry Eoin - ands I don't blame you either!!!!!!!!!

So you said nothing stands out with medications...i.e. no IvIgG?

Had a patient at one place I worked that kept hemolyzing like that and we could not get anything out of the eluate. We decided to "try" transfusing with Jka Negative Units (did not have a non-transfused sample to type) and no more hemolysis (or could be Jkb).

Just another random thought in an otherwise bizzare case.

Brenda Hutson