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Interesting Case Study


cthherbal

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An interesting case:

1st time patient: A neg, negative screen. Transfused 1unit leukoreduced RBCs 2/4. On 2/17 a new sample, screen positive: Jka and HLA identified by reference lab. Re-crossed original unit with new specimen (unit was Jka neg and it was still compatible). We repeated original screen: still negative. 30" incubation: still negative. Could this be a immune response causing a resurgence of previously ID'd antibodies? (That were unknown to us) I can't think of any other reason.

-Colleen

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Hi Colleen,

This is a well-known, but, nevertheless, quite rare phenomenon.

I don't know why it happens, unless the very fact that someone receiving a transfusion may "tickle" their immune memory cells just enough to send them into a frenzy (I suspect that I could have put that more scientifically, but the language echos my shallow knowledge of immunology)!!!!!!

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I'm with Malcolm on this one. I've seen it once or twice. The antibody drops below detectable levels and just that act of getting transfused seems to kick the immune system into gear even with out the offending antigen being present and the titer of existing antibody(ies) goes up. Isn't the human body an amazing machine! :disbelief

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Could this be a response to a transfusion before the patient was seen by Colleen and crew, popping up to detectability sometime between the two specimens? What was the transfusion history before the initial specimen was drawn? A delayed reaction seems more common than the once or twice in a lifetime immune jiggle.

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Or could this be a weak antibody and the first specimen was when the patient was really well-hydrated making it diluted? This could only happen if the antibody was right at the threshold of detectability and a tiny bit more dilution made it too weak. Then there is always passive antibody--any IVIG in the history? Or a previous immunosuppression that has worn off? Or some other cause of generalized immune stimulation?

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Saw this in my blood bank. ID'd an anti-K in a trauma patient, who then received two K-neg units, crossmatch-compatible with PeG (our main method at the time). About a week later, new type and screen is submitted and we ID an anti-K and now an anti-Jka, and DAT is weakly positive. I did a workup -- repeated the old panel with ficin (lucky we had run the Immucor Panocell-10 w/ficin-treated originally!), only anti-K demonstrating in previous sample. Crossmatched the two units transfused, compatible with old sample, one was heterozygous for Kidds and was incompatible with new sample. Eluate positive for anti-Jka.

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Saw this in my blood bank. ID'd an anti-K in a trauma patient, who then received two K-neg units, crossmatch-compatible with PeG (our main method at the time). About a week later, new type and screen is submitted and we ID an anti-K and now an anti-Jka, and DAT is weakly positive. I did a workup -- repeated the old panel with ficin (lucky we had run the Immucor Panocell-10 w/ficin-treated originally!), only anti-K demonstrating in previous sample. Crossmatched the two units transfused, compatible with old sample, one was heterozygous for Kidds and was incompatible with new sample. Eluate positive for anti-Jka.

Yes, anti-Jka is notorious for responding anamnestically; that is why it is such a dangerous antibody, and, on its own, is a very good argument for patients carrying antibody cards.

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We worked it up as if it were a possible delayed. The only suspicious finding was the new antibody that had appeared to develop. We ID'd anti-Jka and had a few cells with extra reactivity. Did not appear to be an anti-Jk3. Reference lab ID'd anti-JKa and HLA antibodies.

DAT and eluate (on post-transfusion sample) were both negative. We had changed screening cells between old/new samples but even when we repeated the old sample with new screening cell the Ab screen was negative. Crossmatch on unit (Jka neg) still compatible with both samples. Will have to store this in my memory banks for when it happens again. Thanks everyone for sharing your thoughts! :D

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...... someone receiving a transfusion may "tickle" their immune memory cells just enough to send them into a frenzy .......QUOTE]

Love your descriptive explanation, Malcolm!

Good points made by Malcolm, John, Phil, Goodchild & Mabel! (I've seen this phenomenon, too.)

Donna

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We had a dialysis patient years ago that never got anything but Rh neg blood. One day she pops up with an anti-D. I researched intensely, looking at LW and anything else I could think of. I never really found an answer, but I wondered if it could have been some minimal antigenic exposure via the dialysis machine to some other patient's D pos blood. Now I wonder if it was this phenomenon.

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This has happened to us twice this year. Once with an Fya and once with a Jka. I am thinking it was secondary reponse, but extra vascular obviously. In the secondary both IgM and IgG are made initally but IgG rises much faster and at a higher titer,then drops off dramatically. Which is why just one unit does the trick in my book.

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Yes, anti-Jka is notorious for responding anamnestically; that is why it is such a dangerous antibody, and, on its own, is a very good argument for patients carrying antibody cards.

Malcolm, If I ever develop a BB antibody, I am getting a medical alert tag!!

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Saw this in my blood bank. ID'd an anti-K in a trauma patient, who then received two K-neg units, crossmatch-compatible with PeG (our main method at the time). About a week later, new type and screen is submitted and we ID an anti-K and now an anti-Jka, and DAT is weakly positive. I did a workup -- repeated the old panel with ficin (lucky we had run the Immucor Panocell-10 w/ficin-treated originally!), only anti-K demonstrating in previous sample. Crossmatched the two units transfused, compatible with old sample, one was heterozygous for Kidds and was incompatible with new sample. Eluate positive for anti-Jka.

Ah, an antibody on a trauma patient. Always fun! :cries::cries:

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  • 1 year later...

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