John Eggington

I just answered this question. My Score FAIL

Could be anti-A1, from the platelet plasma (from A2 donor, with anti-A1), but why no reaction with reagent A1 & B cells (if all tests done by IAT)?

We're all all of the tests of the eluate performed by IAT, including tests against reagent A1 and B cells?

On high dose therapy I would have thought it would be detectable very soon after therapy started (immediately?), but working in a reference lab we're rarely that close, in time, to the start of therapy. It could be mistaken for a warm autoantibody or an antibody to a high frequency antigen but, in my experience, it would seem unlikely it could be mistaken for a 'cold' antibody.

Gestational age also has an impact, I.e., the more premature a baby is the more likely you are to see this phenomenon

How long would you extend the crossmatch/antibody screen for a patient that didn't have antibodies, hadn't, been transfused in the last 3 months, wasn't pregnant, etc.? I suppose this is about how reliable a 'history' you have!

The 'DAT neg', 'auto pos', gal auto antibodies are almost always best managed by using a tube technique. The autoantibody may well bind during the tube incubation phase but is eluted away during the wash phase. You usually find that if you do a gel DAT, but add patient plasma to it and incubate like an IAT, the cells will be IgG coated.

The strength of a DAT can depend on where you take your red cell sample from (of the centrifuged patient simple); sampling from the 'bottom' can give a stronger reaction. With 'minor' populations of DAT pos cells I sometimes fin a tube DAT is better to see a pos population, using an inverted microscope (with a stage adapted to receive the test tube), but I am prone to 'old school' techniques!

I wondered this too, but the patients don't seem to be particularly anaemic, which is what I'd expect if red cells were being destroyed. Maybe antigen is being removed without red cell destruction? Just had a new 'cd38' case and this one has a positive DAT', with therapy starting only a week or so ago. DAT wasn't done before therapy started. Titre of the antibody is almost 4000.

What you say, Mabel, could well be the case. The (limited) published work implies that the patients will be DAT positive, but my (again, limited) experience is that they are DAT negative (and remain so). Could the apparent lack of cd38 on patient red cells be the effect of a prior therapy (the use of gel cards (and other results) rules out 'insufficient washing' , and 'prozone' doesn't 'fit')?

Maybe C and E typing would help? If the patient is C and E negative they're unlikely to be weak type 1, 2, or 3. The ethnic mix of you patient population would effect the usefulness of this strategy.

The failure of adsorption is probably a mix of the high titre of the antibody (in the 'thousands' if a the high dose is given) and a lowi density of cd38 on red cells used for adsorption. Maybe if you spent a week adsorbing the same sample you'd get rid of it! As for how common the phenomenon is; I would have thought you'd find it every time you looked for it, so maybe it's just that the test isn't requested after therapy starts, in a lot of the patients. I still wonder why the auto/DAT is negative in some patients; maybe the DAT positive ones already had a positive DAT before the therapy started?

In answer to Malcolm; I'm sure your right! I was thinking more about how a lab would confirm a genotype result; even if they had the capacity to genotype themselves (where confirmatory testing is required). What could they test?

If donor 'genotyping' is introduced, what impact would this have?

Although foetal cells are bigger they're less dense, aren't they, so they'd more likely be at the 'top' off sample? But a pretty moot point, I know, if the patient is only '4 weeks'.