lacs

Phew! I was worried! I never saw it the last time I renewed. I am good then. Thanks ALL. You guys are great!

Thanks ALL for the reply. What do you do about getting credits for the following areas? a)Research and Preparation for Presentation Authorizing a book or book chapter, doctoral dissertation c) Editing a book d) Presenting posters/exhibits e) Journal articles, master thesis f) Serving on examination committees, committes or boards related to the profession g) Role of on-site inspector/paper reviewer for laboratory accreditation (JCAHO, CAP, etc,) or training program accreditation (NAACLS, CAAHEP) 2pts/year. I don't know about you but I don't have opportunity or able to participate in all of them. Help!!! Aren't we supposed to full-fill all of them??

Does anyone know if we are required to participate in the CMP program if you're an SBB, or is it really optional?

2 homos to rule in and out.

We normally wait for 24hr of continuous monitoring before using it again. Rarely, we use 4hr time-frame.

We do one from for a batch (for example, if they request 2) and we write the unit # on the form.

Somewhat related topic, does your SOP tell you to test for endpoint when adsorb using auto cells? If not, how do you know when to stop? How long do you incubate if you test your plasma against DTT-treated red cells in tube? I want to say 30min (similar to saline) since there is no enhancement but I've not been able to find literature to say exact time.

Unless our patient is also a sickler, we still adsorb. We do PEG adsorption. It's only because we want to save phenotype matched units for those who truly need them, due to shortage of good red cells.

We run 3 screens-one w/o enhancement at IS, 37 and Coombs, PEG and GEL. Our problem is when it only reacts in GEL and looks like HTLAs. We are limited to what is tested. We do ficin, cord in gel and rarely DTT or titer since titration result is typically higher in gel than tubes. How are you all handling reactions in GEL only?

That sounds logical! Thanks you all for responding.

Thanks for the info. Hmm let me double check the PIs they sent us. I am almost 100% certain that it requires unbuffered saline for antisera. No, we're not in Canada. We're in the US.

We are considering purchasing the partial D and competency kits as well. Our local hospitals do not seem to like their ABO/Rh kits. Reactions come off "sticky". Also, we are using buffered saline and their antisera requires unbuffered saline. How are you guys handling that, if you currently are using buffered saline cubes?

Since we're on the same subject. We just had a female patient (much older than a typical childbearing age) who has anti-D and C in her plasma but we were able to dilute anti-D and C in eluate as well. We ruled out passive antibodies. Is it a stretch to think the she received rG at some point and attaching to rG cells from current transfusion? This is still a rare situation. It's almost always an academic interest for us so we hardly work up samples like this, unless there is a good reason to do so, due to costs. What else could it be?

Do you report of cold antibody based on 4C testing only? AKA, no other reactions at IS or RT.

One more question, Our Fy(a-b-) cells came up with ficin. That's odd. Fy3 is resistant to ficin but it should not come up if it's not there to begin with. Any thoughts. One another subject, if you have a typical WAA but is reacting at IS and 37 and RT and 4C, do you call it WAA broad thermal amplitude or mix of cold and warm?

Thank-you both Rh-fan and Malcolm. This is why I am active on this site, to get inputs from experts like you:)

We have a 28 yr old female African American patient who reacted with all red cell samples tested, except for Fy(a-b-) cells. Auto controls were only positive with GEL and saline. DAT + W/AHG,IgG. Eluate was negative. Her reactivity was weaken by ficin. Original thought was anti-Fy3 and not Fya and Fyb since anti-Fya and Fyb would be destroyed by ficin. This patient has a typical Black type Ro K-Fya-Fyb-Jkb-S-. We're sending the sample out for genotyping. If she has GATA mutation, she can still make anti-Fy3 and anti-Fya. It's extremely rare for a Black patient to make anti-Fy3. It's usually mistaken for anti-Sla. We decided to perform testing against DTT treatment of red cells and checked against the patient's serum- Result was negative. This information tells us it might be something in the Knops system. We are still validating trypsin so can't test that. Sla would be sensitive to Trypsin while anti-Fy3 is resistant. Are we heading in the right direction? What are your thoughts?

AMcCord, Is this question for me?

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

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.

Hi Shily, It is correct but Bg antigens are leukocyte antigens of low incidence.

Thanks Malcolm for "interpreting" for my short-handwriting. I wanted to shorten it but at the end made it more confusing. Our Medical Director is looking into the patient's medical conditions and history. Perhaps that will shed some light on this case.

Hi Shily, The patient is Rh+. We ruled out D-variant, LW and passive anti-D. Where would allo-anti-D come from then? The patient does not have ITP with WinRho administration.

Would we be able to eluate anti-I in the eluate? How do we explain the D pattern then?

Hi Anna, Sorry for my abbreviations. It's a long case and I wanted to shorten it:) The patient's DAT is positive. What I meant above was that patient’s EGA-treated DAT negative reacted with his/her eluate and plasma. This proves that what we see in the plasma and eluate is WAA. What we don't understand is that anti-D is left behind when adsorbing with Rh-phenotype similar red cells. In our experience, WAA with a specificity would be removed by either antigen positive or negative against that specificity. Also, this D pattern comes and goes. We ruled out LW even though cord result points toward it.