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Multi-racial patient in May 2011 APOS, R1rK-Fya-Jkb-S-, reacting with all cells, including auto, and reacting stronger w/D+ cells.

Eluate pan-reactive w/all screen cells in tube.

Patient’s DAT negative reactive w/eluate and plasma=WAA

D typing w/BioClone 4+ IS; 3+ W/Immucor/Gamma

Adsorption w/Rh- cells left behind D

Panel against Cord cells (to rule out LW)-negative

DTT treatment of red cells against adsorbed plasma–stayed positive-true D.

Aug 2011, reactions match a typical WAA exactly. Removed w/Rh+, pheno-similar

Sept 14 workup-

Looks like a warm.

Adsorbed against Rh looks like anti-E and D, Lua left behind.

Is this WAA w/D-variant? Anti-LW or WAA w/D, E and Lua? Why was D disappearing w/2nd workup? Patient is Rh+

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Multi-racial patient in May 2011 APOS, R1rK-Fya-Jkb-S-, reacting with all cells, including auto, and reacting stronger w/D+ cells.

Eluate pan-reactive w/all screen cells in tube.

Patient’s DAT negative reactive w/eluate and plasma=WAA

D typing w/BioClone 4+ IS; 3+ W/Immucor/Gamma

Adsorption w/Rh- cells left behind D

Panel against Cord cells (to rule out LW)-negative

DTT treatment of red cells against adsorbed plasma–stayed positive-true D.

Aug 2011, reactions match a typical WAA exactly. Removed w/Rh+, pheno-similar

Sept 14 workup-

Looks like a warm.

Adsorbed against Rh looks like anti-E and D, Lua left behind.

Is this WAA w/D-variant? Anti-LW or WAA w/D, E and Lua? Why was D disappearing w/2nd workup? Patient is Rh+

Hi Malcolm,

I don't have the exact info, but we use Immucor AHG, IgG and C3 for all WAA workups

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Hi Malcolm,

What about the D pattern after adsorption with D- cells then? It comes and goes.

Yes, that's the bit that is giving me acute brain ache!

I would think that the answer could be as simple as the auto-antibody is mimicking an anti-D, is then broadening in specificity, and then narrowing again, and so on, depending upon the patient's condition; but it may also not be that simple!!!!!!!!!!!!!!!!!!!

:confuse::confuse::confuse::confuse::confuse:

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Yes, that's the bit that is giving me acute brain ache!

I would think that the answer could be as simple as the auto-antibody is mimicking an anti-D, is then broadening in specificity, and then narrowing again, and so on, depending upon the patient's condition; but it may also not be that simple!!!!!!!!!!!!!!!!!!!

:confuse::confuse::confuse::confuse::confuse:

Thank-you Malcolm,

I am sticking to that theory also since we ruled out ITP, passive antibody and D variant.

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I am very interesting in this post, but because my English is not so good, I can't understand it well.

I have difficult to understand what is the meaning of APOS, w/D+ , plasma=WAA,pheno-similar.

Help is expected, thanks in advance!

I agree (as also not englisch speaking by nature), the start of this topic was a little bit hard to read because of the short hand writing.

According to sugestion af the 'allo' anti I, I would have aspect that the antibody was also reactive at lower temp (and I see only report of warm antibodies) and it dont explane the positive DAT (although that could also be something else).

You have used to anti D reagents, is that how you ruled out an RhD variant?

I agree with Malcolm that "mimicking" is the only explanation for the come and go af the antibody, that suggest an auto antibody (LW or D does not matter)

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I am very interesting in this post, but because my English is not so good, I can't understand it well.

I have difficult to understand what is the meaning of APOS, w/D+ , plasma=WAA,pheno-similar.

Help is expected, thanks in advance!

shily, both you and Rh-fan are right - we do use an awful lot of "jargon", and sometimes even people who speak English do not understand one another - particularly when one is speaking UK English and the other US English!!!!!!!!!!!!

APOS probably means group A, D Positive (for someone who, like me, also does not like this terminology, read Peter Issitt's books!), w/D+ probably means Weak D (Weak D+ means nothing, as there is no such thing as anti-Weak D), plasma = WAA probably means the plasma contains a warm auto-antibody, and pheno-similar means that blood was given that was not positive for an antigen within the Rh Blood Group System that the patient themself lacks - for example, an Rir patient would be given E- blood, but could be given R1R1 or rr blood, both of which are E-, but neither of which is Rh identical.

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According to sugestion af the 'allo' anti I, I would have aspect that the antibody was also reactive at lower temp (and I see only report of warm antibodies) and it dont explane the positive DAT (although that could also be something else).

But an alloanti-I can have a wide thermal amplitude, and not just be detected in the cold. I thought that, in the original sample, the DAT was negative?

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Malcolm, you are a good teatcher, you explain it very clear, thank you very much.

I think there is a strange result is the DAT, it is neg, but the auto is pos and the eluate is pos,too.

I don't know the pos result is how strong, if it is weak, maybe because the antibody on the auto cells is too less to react in the DAT, and auto will add 2 drop of plasma and incubation to strengthen the react, and eluate will let the antibody in a less volume liquid to strengthen it too.

Sorry, I am not agree with the result of allo anti-I, because the pos auto and eluate.

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If the eluate is equal strength to all panel, I prefer the anti-D is alloantibody, because the plasma reactive stronger with D pos cells, if it is autoantibody show anti-D specificity, the eluate will show the same reaction.

I think it is autoantibody add allo anti-D.

Just a guess, if it is not right, please point it out, thanks.

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Can I just see if I have understood correctly? Your patient is reacting (I presume in Coombs) to all panel cells and his own auto control, but cord cells are negative and his DAT is negative?

Hi Anna, Sorry for my abbreviations. It's a long case and I wanted to shorten it:)

The patient's DAT is positive. What I meant above was that patient’s EGA-treated DAT negative reacted with his/her eluate and plasma.

This proves that what we see in the plasma and eluate is WAA. What we don't understand is that anti-D is left behind when adsorbing with Rh-phenotype similar red cells. In our experience, WAA with a specificity would be removed by either antigen positive or negative against that specificity. Also, this D pattern comes and goes. We ruled out LW even though cord result points toward it.

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If the eluate is equal strength to all panel, I prefer the anti-D is alloantibody, because the plasma reactive stronger with D pos cells, if it is autoantibody show anti-D specificity, the eluate will show the same reaction.

I think it is autoantibody add allo anti-D.

Just a guess, if it is not right, please point it out, thanks.

Hi Shily,

The patient is Rh+. We ruled out D-variant, LW and passive anti-D. Where would allo-anti-D come from then? The patient does not have ITP with WinRho administration.

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Thanks Malcolm for "interpreting" for my short-handwriting. I wanted to shorten it but at the end made it more confusing.

Our Medical Director is looking into the patient's medical conditions and history. Perhaps that will shed some light on this case.

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Hi Malcolm,

We wouldn't be able to elute if off if WAA is IgA, would we?

Well, yes you would, but the important word in my post was "largely", because there is usually some element of IgG there as well, and, although you may not be easily able to detect this by DAT, as shily says, the elution technique has the ability to "concentrate" any antibody on the red cell surface, and so you may well be able to detect this in the eluate (thus making the entire case even more confusing!!!!!!!!!).

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Would we be able to eluate anti-I in the eluate? How do we explain the D pattern then?

This is quite a complicated concept, but I'll have a go at explaining it (and probably completely mess it up - but here goes anyway).

Early in the production of human IgM anti-D, if you catch it just at the wrong point in time, the anti-D is so poor at being specific it can mimic an anti-I. This is because there is a short part of the D molecule that shares moiety with the I antigen (I can't immediately put my hand on the paper about this - it is buried in the rest of the detritis on the desk in my office, but I will try to find it. It won't be straightaway though, because I'm lecturing all this morning) and, as you know, IgM antibodies made straight after primary response have a "wider specificity" than do later IgM molecules and IgG molecules.

This was also true of many monoclonal IgM anti-D reagents in the early days (and may still be so, for all I know), and this was why it was always recommended that these reagents be brought up to room temperature before use - so that no false positive reactions were detected with I antigen in the cold when the patient was actually D negative.

Now then, if your patient has continued to make this particular specificity (rare, but not unknown), it is entirely possible that this single antibody will react with all I positive red cells, but that this single antibody will have a greater affinity for D+ red cells. This would also explain why the "anti-D-ness" of the antibody comes and goes, with the condition of the patient.

This explanation is in no way a "definitive answer" to this complex case, but it cewrtainly is something to think about.

Mind you, of course, this goes entirely against my earlier theory that it may be an alloanti-I in an adult ii!!!!!!!!!!!!!!!!!!!!!!!!!!!!

:no::no::no::no::no:

Edited by Malcolm Needs
Afterthought.
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