O neg with Ant-c?

[Barb Thompson]

Hi, we just had a patient who is O neg, is c-positive, and has a perfect Anti-c in his plasma.  He claims to have never had a blood transfusion. His current diagnosis is "Incarcerated Ventral Hernia", but had been treated for colon cancer 17 years ago.  The surgeon won't take him to OR unless we have blood available.  His DAT is 3+, Anti-c eluted from his red cells.  No unusual meds.  I'm thinking Warm auto mimicking anti-c.    Reference is sending out  for molecular genotyping because they are thinking he may have a little c variant and this is an alloantibody (he is white, and has never been transfused).  Any thoughts on this?

[Yanxia]

Have not been transfused, and DAT is pos. If this anti-c can be absorbed out by his own cells, then it is  auto antibody.

Edited May 11, 2016 by shily

[Malcolm Needs ☆]

I think a warm auto-antibody mimicking anti-c is much more likely than an allo-anti-c as a result of a c variant, particularly with the results you are getting with the DAT and the eluate.

[SMILLER]

I would think that variant c antigen or no, a patient is not going to make an antibody against ANY of his own antigens under normal circumstances.  So I agree with Malcolm (not that I would ever disagree!)

Do we not just give c negative blood to this patient?

Scott

 

[Malcolm Needs ☆]

I think the key to what blood should be given (if, indeed, the anti-c is an auto-antibody) is whether or not the patient expresses the C antigen.  If he does, then I would be happy to give c negative units of blood.

If he does not, however, I would give c positive blood, because, if he makes an allo-anti-C in addition to an auto-anti-c, finding any blood for him would be almost impossible.

Your first sentence is of interest.  This is true (in most cases), but an individual who is d(C)ce^S or DIII(C)ce^S, can make a true allo-anti-hr^B that mimics an anti-C+e, and an individual who is hr^S negative can make a true anti-hr^S that mimics an anti-f, even though they may apparently express c and e in the cis position.  However, such mutations are, to all intents and purposes, only found in the Black populations of the world.

[SMILLER]

Is there such a thing as an auto-antibody that truly only mimics an anti-c?  Or would it have to be some really rare epitope actually related to the Cc/Ee system?

Scott

[goodchild]

Isn't O Neg, c-neg blood ludicrously rare?

[Malcolm Needs ☆]

52 minutes ago, SMILLER said:

Is there such a thing as an auto-antibody that truly only mimics an anti-c?  Or would it have to be some really rare epitope actually related to the Cc/Ee system?

Scott

Well, yes and no!  Sorry to be obtuse Scott!  An anti-f, in itself, can mimic an anti-c (whether it is an allo or an auto antibody) because, if the antibody is weak, it may not necessarily react with examples of r'r, r"r or r_yr, R₁r, R₂r or R_zr, because the f antigen has heterozygous expression on these red cells, whereas a true anti-c will not necessarily show agglutination (for a similar expression of the c antigen) with the r'r, r_yr, R₁r or R_zr red cells - this is, of course, ignoring really rare Rh types involving the "stranger" mutations.

[Malcolm Needs ☆]

56 minutes ago, goodchild said:

Isn't O Neg, c-neg blood ludicrously rare?

Yes, but not unknown by any means.  We have quite a few units frozen down in the UK, and I would have thought, the same applies to the USA and The Netherlands - although not Japan.  The thing to remember is that, although the donors might be ludicrously rare, so are the patients that would require such blood.  It's a situation where the donors almost cancel out the recipients (if you see what I mean).  I think I could have put that an awful lot better!!!!!!!!!!!!!!!!

[Barb Thompson]

The patient is rr.  Reference reported it as "unidentified antibody with anti-c specificity".

[Malcolm Needs ☆]

Hmmmmmmm, not the most useful Reference report I have ever read!

Does this mean that they have not determined whether the anti-c is a straightforward auto-antibody, or whether it is the result of some kind of mutation in the RHCE gene, and that the antibody is an allo?

Sorry, but this is important.

[SMILLER]

18 hours ago, Malcolm Needs said:

Well, yes and no!  Sorry to be obtuse Scott!  An anti-f, in itself, can mimic an anti-c (whether it is an allo or an auto antibody) because, if the antibody is weak, it may not necessarily react with examples of r'r, r"r or r_yr, R₁r, R₂r or R_zr, because the f antigen has heterozygous expression on these red cells, whereas a true anti-c will not necessarily show agglutination (for a similar expression of the c antigen) with the r'r, r_yr, R₁r or R_zr red cells - this is, of course, ignoring really rare Rh types involving the "stranger" mutations.

Malcolm, so is it possible that this patient is making auto anti-ce? (or anti-f, or anti compound ce -- whatever you want to call it!0

Scott

[ltechlin]

14 hours ago, Barb Thompson said:

The patient is rr.  Reference reported it as "unidentified antibody with anti-c specificity".

Does your report give a transfusion recommendation?

[Malcolm Needs ☆]

34 minutes ago, SMILLER said:

Malcolm, so is it possible that this patient is making auto anti-ce? (or anti-f, or anti compound ce -- whatever you want to call it!0

Scott

It certainly is possible, as auto-anti-f has been reported (see, for example, Reid ME, Lomas-Francis C, Olsson ML.  The Blood group Antigen FactsBook. 3rd edition, 2012, Academic Press, page 211).

[SMILLER]

That's all good and somewhat interesting. The thing is though. what do we do for the patient?  Just give them ce neg blood?  Because they did have a rather strong DAT and  Barb's reference lab reported it as  "unidentified antibody with anti-c specificity".  I would appreciate another post from Barb letting us know how it was handled.

Scott

[Malcolm Needs ☆]

Well, the patient should be given D Negative blood, as he is rr, so that he does not make an anti-D (which is MUCH more clinically significant than would be an anti-f.  This means that, if you are going to give him f negative blood, the units would need to be taken from a donor who is r'r', r"r", r_yr_y, r'r", r'r_y or r"r_y - all of which are disappearingly rare, and so, to be pragmatic, and as anti-f has only been implicated in mild, delayed haemolytic transfusion reactions, no, I would not give f negative blood (but it might be worthwhile just covering him with IVIG).

[Barb Thompson]

The patient had his hernia surgery on Wed May 11.  His post-op Hgb was 16.  He does not appear to be experiencing a hemolytic process, although no testing was performed (no LDH, haptoglobin, retic, etc).   His TBil was slightly elevated at 1.8.  It does not look like a hem/onc has been consulted.

Reference did not give any recommendations as to what type of blood to give, should he need a transfusion.  We are still waiting for the results of the molecular typing. 

Anesthesia was funny (funny-sad) - I was trying to explain that we would not have compatible O negs for the patient, and she replied that she would just take trauma blood, then. As if that would solve all the problems. Thankfully, he did not need a transfusion.

My theory (and it's just a theory) is that this is a warm auto, caused by a yet-to-be-diagnosed malignancy. Possibly his colon cancer has returned.  Did I mention he is 82?

Barbara

[Malcolm Needs ☆]

40 minutes ago, Barb Thompson said:

My theory (and it's just a theory) is that this is a warm auto, caused by a yet-to-be-diagnosed malignancy. Possibly his colon cancer has returned.  Did I mention he is 82?

Barbara

Thank you so much for updating us on this patient Barbara.

Although malignancies can lead to the weakening or loss of a number of Rh antigens, such weakening or loss are usually seen in cases of myeloid leukaemia, polycythemia, and other myeloidproliferative disorders (in other words, haematological malignancies), rather than, for want of a better way of putting it, solid organ malignancies, so, whilst I agree with you that this does seem to be a warm auto, I think it much more likely that it has been caused by a "leak of bacteria" from the gut (following his colon cancer, or, indeed, his hernia), rather than as a primary symptom of his previous alimentary tract pathologies.

I am, however, happy to be proved wrong!!!!!!!  It wouldn't be the first time, and would probably not be the last!

[SMILLER]

There is a thing about developing odd antibodies to RBC antigens with colon cancers if I am not mistaken (or is it odd antigens on RBCS?)  Not sure about anti-c-like stuff though.

Would be interested in what the molecular testing comes back as.

 

Thanks, Scott

[R1R2]

What enhancement media are you using for your screen/antibody ID? 

[SMILLER]

On 5/12/2016 at 8:49 AM, Malcolm Needs said:

 (but it might be worthwhile just covering him with IVIG).

Malcolm

This got my attention because although I have heard of using IVIg for various ailments, I was never really sure exactly how it works.  So this is off-topic here a bit but after all of my exhaustive, extensive research (wikipedia), I have to ask: how would this work in this situation? (or at least, how might it work?)  I am thinking that the pool of Ig would have to contain lots of anti-c?  Or is it just the general auto-immuno-suppressive effect that would make it safer to transfuse this patient?

Thanks, Scott

Edited May 13, 2016 by SMILLER

[Barb Thompson]

We use gel for the antibody screen and ID. The DAT was done in tube. The reference lab uses PeG.

[Malcolm Needs ☆]

23 minutes ago, Barb Thompson said:

We use gel for the antibody screen and ID. The DAT was done in tube. The reference lab uses PeG.

In my humble opinion, they should use the same technology as you used to detect the reaction in the first place.

NOW, I will be honest and tell you, we don;t necessarily use the same technology as the submitting hospital either!!!!!!!!!!!!!!!!

[Malcolm Needs ☆]

32 minutes ago, SMILLER said:

Malcolm

This got my attention because although I have heard of using IVIg for various ailments, I was never really sure exactly how it works.  So this is off-topic here a bit but after all of my exhaustive, extensive research (wikipedia), I have to ask: how would this work in this situation? (or at least, how might it work?)  I am thinking that the pool of Ig would have to contain lots of anti-c?  Or is it just the general auto-immuno-suppressive effect that would make it safer to transfuse this patient?

Thanks, Scott

Well, as far as I know, nobody knows, definitively, how IVIG does work, but it seems to have the ability to prevent SOME transfusion reactions AND recurrence of hyperhaemolysis (particularly if used in conjunction with methylprednisolone), but it doesn't seem to prevent primary stimulation.  It MAY work by feedback to the immune system that it has made "enough" antibody, or may just block the receptors  of the immune system.

As for the amount of anti-c in IVIG?  Well, there is probably some, but I doubt whether there is a lot (in the same way that there is not a lot of anti-D), otherwise giving IVIG would regularly result in mild (at the very least) transfusion reactions.  In the recent past, of course, it HAS been blamed for causing pure red cell aplasia, following an A to O stem cell transplant, because it certainly did contain large amounts of anti-A, but, according to the manufacturers, this is no longer the case.

PHEW - that tested the little grey cells!

[R1R2]

3 hours ago, Barb Thompson said:

We use gel for the antibody screen and ID. The DAT was done in tube. The reference lab uses PeG.

I would be curious if the reactions would go away if saline technique was used instead of gel?