John Eggington
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Posts posted by John Eggington
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Would be interesting to see what was eluted from the babies red cells. Could anti-A bound to twin 1 have blocked binding of some of anti-D and anti-G? Does not sound very lkely, must admit!
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No transfusion, so far. I believe that EPO is being administered. It does seem likely the patient will need transfusion at some point, the clinicians have a bit more time to think about it. Still awaiting full resolution of the D type for 'fully informed' decision. Hopefully we'll have all the information in place before transfusion is required.
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Having said that; of course, you are right, testing any siblings would be a good place to start.
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The best way to describe this a 'Friday afternoon case', so I'm sure that option will be looked in to. The problem here is that it doesn't involve the usual type of rare problem, like a high frequency negative phenotype or a null phenotype, where family members are likely to be good candidates for having the same phenotype.
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Not tried other blood banks, yet. There appear to be only 5 r'r' Fy(b-) K- (all M+) UK donors, all eligible to donate now (most haven't donated since last year). To 'complicate' matters, the patient appears to be a partial D, rather than straight forward D-. The strong DAT pos (eluted anti-c and anti-Fyb), made the ALBA panel results a little difficult to interpret (haven't CD treated cells, just sent it straight to IBGRL). ALBA results make it appear to be a DVI, but (limited) genotyping of D gene, looking for D exons, 1, 5, and 10, shows all 3 are present. So if it is a DVI, it's not a straight foward one! I guess the real problem is, how will transfusion support be managed in the longer term. Maybe it'll turn out there are 2 variant genes, and one is a weak D type 1, 2 or 3 (with even weaker antigen expression because of the 2 Ce genes)!
- Malcolm Needs and Auntie-D
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Patient is D-C+c-E-e+, Hb of 70g/L. Llikely to need on going transfusion support. The patient has had one previous transfusion episode (when no antibodies were detected), about 3 weeks ago. They now have anti-c, anti-Fyb and anti-M (the anti-M is reacting at 37C, but only with M+N- cells, at the moment). There are 2 frozen units that are r'r' Fy(b-) M+N+, after that there are no more r'r' Fy(b-) units. Do you transfuse R1R1 Fy(b-) M- that are fairly easily found, or use the r'r' Fy(b-) M+N+ units?
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Malcom is correct,we have used the 'ALBA' panel of monoclonal anti-Ds. So we've (hopefully) ruled out a few things already.
As for my scouse accent; anyone whose had the pleasure to her my voice will know I haven't managed to pick one up in the 30 odd years I've lived here (although I do have a 'lecky' meter)
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Sorry, meant DIV!
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Resasonably sure it's not DVI or DVII
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We, at Liverpool, suspect mother is DIII but, as Malcolm said, we will need some (sequencing) help from IBGRL to 'pin it down'!
- Auntie-D and Malcolm Needs
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You've said the autocontrol is positive and negative, which is correct?
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What's the diagnosis and what technique do you use for DAT?
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Which phrase Elizabeth? - send me a private message if it is that embarrassing (or email me on Malcolm.needs@blueyonder.co.uk).
With respect to 'Blow me'; this would be the same as 'That's a funny thing' or 'Blow me down', generally 'What a surprise!'
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Patient Blood Group is
Forward: A 3+, B3+, D4+ Reverse: anti A 2+, anti B 2+ Auto Weak+
37: Forward: A0, B4+, D4+, Reverse anti A 4+, anti B0, Auto 0.
E 0, C+, c+,e+ k+-, Jk+-
You give 2 different sets of forward and reverse groups; which set is the patient's result, and what does the other result represent?
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maybe one of the units was Jk{a weak}. Have seen a few and they are VERY weakly positive. Usually spotted when we have tried to report a Jk(a-b-} phenotype!
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Have you tried a 'cold' panel? Also, what's the matter with the patient, have they been transfused, etc.
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Oh dear, John, don't get your nickers in a bunch!
Well, as they obviously are 'bunched', I suppose I should actually say what I might do in this situation;
Firstly, 'weak' is fairly subjective. Variables might include the technique/technology you are using, how your automation is set up, who's performing the test, etc., etc., we all know them. So I'll define 'weak' as 'repeatedly unable to interpret ABO grouping by first line test and subsequent testin by alternate technique(s)' (I'm assuming the first line test will be some form of automated system).
More often than not our 'weak' results are resolved by applying the alternate technique. In my case this will be a 'tube' ABO group. I've worked with people who have variously advised the use of enzyme treated grouping cells, increasing the volume of patient serum/plasma, and lowering the incubation temperature, as additional ways to enhance reactivity.
So, the alternate technique gives 'strong' reactions; is the backgroup still 'weak' enough to require an enhanced antibody screen? We'll each have our own take on that! If it is decided that the alternative technique is still 'weak', and an enhanced antibody investigation is deemed necessary, my approach would be to use alternative techniques, rather than adjust the routine one. For example, you could apply a range of techniques in combination with one another; enzyme IAT, tube IAT (good for detecting weak anti-Fya and anti-Fyb, I find), reducing the temperature, selecting test cell phenotypes you think may offer more sensitivity than the screen profile (e.g., including a K+k- cell, if the screen is K+k+). Some of these techniques may enhance 'insignificant' antibodies but that is always the 'price' for applying enhancements. If these techniques failed to show anything of 'significance' I'd stop, relatively comfortable in the knowledge that if my routine technique (most of which seem almost too sensitive, as it is) and my enhanced combination had failed to find anything, then it's unlikely that anything of immediate significance is present.
Having said this, I would not do an 'enhanced work', on a patient with a 'weak' backgroup, unless the patients condition suggested that an undetectable, clinically significant, red cell antibody was thought to be present, and causing problems.
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Well John, thank you for sharing with us your insight. This is why we all joined PathLab Talk so that we can benefit from the wealth of knowledge and experience from interesting and insightful professionals like yourself.
Joke, for goodness sake!
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Thank you John.
I guess I wanted to know the details of the "Bag of Tricks."
Well now, that would be telling...!
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David,
Thank you for your honest post. You are right, it is entirely possible that a mountain is potentially being made of a mole-hill but when the backtype enhancements are tried and do not enhance the reaction and the patient does not fall into the usual category of an immune-suppressed patient and there is no responsible history attainable for this patient, do we just kiss it up to God and hope for the best or should we be aa little more proactive?
This is not quite how the thread started. I think that most of us responded with respect to what we might 'routinely' do when we encountered a 'weak backgroup'. If we come across scenarios that do not 'add up', Im sure we all have a 'bag of tricks' we go to to further the investigation. I also bet all of our 'bags' are different!
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How to do the saline incubation?
I think we were talking about the 'classic' tube IAT, with cells suspnded in saline and incubated for 30 minutes at 37C. We then seemed to have an argument about something we all agreed on!
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Missing a weak antibody in an immunocompetent patient would be much more significnt than missing one in an immunocompromised patient, I would have thought. . You cold justify applying a 'different' antibody id technique on a patient that gave a positive antibody screen, but every negative you encountered would need the enhanced technique. I would have thought the 'judgement call' would quicky start to fall on the side of 'caution'; who would want to be the first person to miss an antibody due to failure to apply proper judgement?
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I think you'd have to use your 'enhanced' technique on all patients, regardless of backgroup results, once you'd intoduced it. All patients would have to benefit from a more sensitive technique; you can have weak antibodies without having immune supression. I assumed David would do an AHG crossmatch because he hadn't got a vlid ABO result, not because he was worried the abs screen had given a false negative result; I'm sure he'll clarify if I've misunderstood.
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The original idea of this thread needs every sample from every patient to always get a 'reverse group' (i.e. the first and every subsequent sample of any patent), is this the case? Also, where do group AB patients 'stand'?
HDFN in Twins Clinical disparity
in Transfusion Services
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Still need to know what antibodies were eluted from the red cells of both babies. Also, were the monospecific DAT results the same in both twins? Starting to seem possible that twin 1 is a 'weak/variant D'. We've certainly seen 'weak/variant D' newborns (where mother has high level of immune anti-D) with strong positive DAT results, and elutable anti-D, who have supprised us by being completely unaffected by HDFN.