Pony

In looking at your results, there are things I'd rule out before going the hrS route. I'd be more likely to call this an anti-f that may or may not have an auto component to it. I agree the Lua is there. I'm not sure how confident I'd be about -Jka not being there based on your 2 rule out cells. I've been doing quite a bit with -Jka lately and it varies as much on testing platform as it does on dose. That gives me chills. An eluate and triple absorption with R1R1, R2R2, and rr cells needs to be done to see what you can separate.[ make sure one of the abs cells is Jk(a+b-)] If the eluate just reacts with everything, there's the auto specificity with he bulk of it on the patient's cells. Any chance you could separate retics? I'd really hate to commit on this one without a true phenotype. Lots of luck

Malcolm, On hrB, I agree with what you see with C+e+, Immunohematology. 1995;11(3):74-7. I found Ro patients had a nasty habit of looking like -f or -e and then turned out to be hrS. But this is a different population. I was working exclusively with Black patients. though the ones we found of mixed descent were the biggest pain to work with. The Polynesian group will probably have mixed descent folks as well and that will add a new kink to what we know. Or thought we did anyway.

Don't give up the ship just yet. Working at a national ref lab, I've seen more than my fair share of -hrB and -hrS. Did you look at the rest of the phenotype on the 2 R1R1 cells? Any chance the donor could have been black or mixed descent? That would be my kind of bad luck to have 2 such cells in an inventory that carry weak expressions of e. Plus, more of the antibodies I have worked with that are directed at variants, do not react with a predictable strength because we really don't know the availability of the epitopes the antibody is binding with. There is too much variability with single dose cells to be comfortable with using them for exclusion. As long as R2R2 cells are working for transfusion, I agree with Malcolm. Getting the molecular work done could tell you exactly where you stand and add to our body of knowledge.

I so agree with you on the sensitivity issue. 25, 30yrs ago we were not seeing this carp as you so elegantly put it and we didn't kill anyone. The quest to be the most sensitive product method is driving most hospital techs crazy. Like you, when I see a string of positives in gel or solid phase that do not react in PEG or LISS and show no specificity I KNOW IT WON"T HURT ANYONE IF IGNORED. I have not seen a single case of "unidentifiable reactions" in gel or solid phase cause a serologic reaction let alone an DHTR. I swear the paranoia about "not missing a clinically-significant antibody" has been fostered by the manufacturers trying to expand their business base. Yes, if you have a weak Kidd or Duffy, it may well show up first in gel or solid phase and that is an advantage. But if if you don't see it until the patient has had a unit or 2, worst case scenario is a positive DAT, with future transfusions being antigen-negative. The patient never notices. One of the cost issues is that once a positive reaction is reported in an antibody screen BB LIS here in the US, it will mandate a full crossmatch. That is a waste of time and money. At present, between SOPs and software, we have painted ourselves into a corner with these nonspecific reactions. Are we doomed to each slog through coming up with institution-specific testing algorithms or can we get some solid numbers published through lookbacks to show how oversensitive we are being? What do the rest of you think?

Malcolm - I think we do have a confusion of names here. When I say weak D, I mean what we used call Du. When I'm talking about D variant, I mean those situations where the various genetic mix and match produce antigens which are missing epitopes. There was quite a debate about this at the Baltimore AABB. Joyce wasn't there but Geoff Daniels was. We walked away from that thinking we were all on the same page. But it sounds like your side of the pond is calling everything a D variant? Is that what's happening?

Mabel - this is a fascinating case and really should be written up. The Ref lab that sorts out the D variant will help you. I'd talk to Connie Westhof at NY Blood Center about this one. She's got the resources to do a really good job for you. As to your unexpected titre results - remember this is not a normal anti-D you are working with. It's aimed at the part of the D your patient is missing. The steric hinderence issue could very well be part of how well and how effectively the red cells are able to bind antibody. That may come clearer when the D variant work is completed. The presence of anti-G and -C just adds to the general confusion. My rule of thumb on giving RhIg to patients who have some D on their cells has always been give it to D variants if it can still modify the immune response (ie anti-D titre 2048 is past hope). The downside to this is the positive DAT after the fact. It makes your followup investigations more complex and you never know how long and how much RhIg has been in circulation to be effective. Your medical director is likely to have the best idea of how much serologic risk the local OB docs can handle. For weak D patients, I've always thought it is a total lost cause as these patients have completely normal D on their red cells, just less of it. These are the least likely to make anti-D. These are just my opinions and with a dollar, might get you a coffee. I'll be waiting eagerly to hear how this case goes and what you find out. Best of luck!!

Good point John! What I found out when talking to Georgetown was that the manufacturers' really just count on the dilution to weaken the extra antibodies while adding to the concentration of anti-D. the anti-C, -E and -G just happen to be present more often than the others so they don't dilute quite as much. And for the majority of rr prenatals, it's a moot point.

Yes -RhIg contains anti-C, -E, G and quite a few more of the common string of antibodies depending on lot. The primary antibody with the highest titre is anti-D by a long shot. This was presented at the last Philly AABB as an oral poster from Georgetown University Hosp. I think the paper came out in Transfusion shortly afterwards. All testing to identify antibodies other than Rh was performed by solid phase. In tube LISS, the main 3 identifiable were anti-D, and slightly weaker anti-C & -E. Consider where the product comes from - large pools of plasma from immunized donors (a lot of them multiparous women) as long as the major component is anti-D, it will get the job done. When using it for TTP, the other specificites may help with blocking the destruction of platelets. It is a very valuable tool!