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:

Thank-you Malcolm!!!! That was a very interesting concept. We'll keep an eye on this to see how it develops. It does make a little more sense than what we saw. I don't have the paperwork with me right now but I'll check again. Thanks for your help! Two heads are better than one (actually there have been many heads:)....more to update when I have more information.

Iacs, Do you have a drug history for this patient? Even if he has not received IVIg there are some drugs that can cause anti-D like reactivity. Did you try doing a super-DAT?

Could you elaborate on the 'other drugs', please? thanks

Would it not be worth trying the untreated serum against a panel of enyzme treated cells and untreated cells at different temperatures? I'm still concerned that the panel against cord cells was negative

Would it not be worth trying the untreated serum against a panel of enyzme treated cells and untreated cells at different temperatures? I'm still concerned that the panel against cord cells was negative

Are you thinking in terms of an auto-anti-HI Anna, after all, the patient is a group A?

Would it not be worth trying the untreated serum against a panel of enyzme treated cells and untreated cells at different temperatures? I'm still concerned that the panel against cord cells was negative

Good suggestion Anna. Our sample is old but been refrigerated. I'll see how much we have left at this point.

AMcCord,

Is this question for me?

AMcCord,

Is this question for me?

Sorry for not being clear....the question is for Christyn reference the drugs associated with Anti-D like reactivity.

Interesting case - thanks for sharing.

Are you thinking in terms of an auto-anti-HI Anna, after all, the patient is a group A?

Hi Malcolm. I haven't got that far. I just get the impression that there's an important piece of information missing in this puzzle , but need more clues -

Anna

I read that Anti-Vel(not sure) react stronger with D+ cells then D- cells. could this be it?

I've never heard of this phenomenon, and, certainly, Geoff Daniels does not refer to it in his book. If it were true, I'm certain that Geoff would have mentioned it.