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jojo808

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Patient has the following antibodies: (Pt is B+)

Jk3, E,c, He phenotypes K, Fya, S, N negative. Our ref lab found us 2 units that are phenotyped matched, one B+ and one O+ rbc. They are both incompatible, the O+ is 1+ in Gel, the B+ +/-.

Auto control Neg, DAT neg (reference lab results). What's our next step??? BTW hope you all are doing well during this time. 

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This is an almost impossible question to answer, as it is ALWAYS the responsibility of the physician looking after the patient to perform a risk assessment as to which he or she thinks is the higher risk - viz is it a higher risk to go ahead with the transfusion, or is it a higher risk to leave the patient without a transfusion?  He or she will take advice from such professionals as the Pathologist, but, in the end, only they can take the decision.

That having been said, it also depends whether any or all of those antibodies listed are detectable in the present sample, or whether some are historic, and, therefore, if some of these can be "ignored" from the point-of-view of transfusion, such as the anti-N.  In extremis, the clinical significance of the antibodies can be assessed by use of bioassays, such as MMA, ADCC and CLT, and even looking at the IgG subtypes of the antibodies.

If it is decided that it is safer to go ahead with the transfusion, than to withhold the transfusion, it could be made safer by  the use of IVIgG (see, for example, Win N, Needs M, Thornton N, Webster R, Chang C.  Transfusion of least-incompatible blood with intravenous immunoglobulin plus steroids cover in two patients with rare antibody.  Transfusion 2018; 58: 1626-1630 [doi: 10.1111/trf.14648], and Win N, Almusawy M, Fitzgerald L, Hannah G, Bullock T.  Prevention of hemolytic transfusion reactions with intravenous immunoglobulin prophylaxis in U- patients with anti-U.  Transfusion 2019; 59: 1916-1920 [doi:10.1111/trf.15230]).

Finally, I MUST remind readers that I am a (retired) Biomedical Scientist, and NOT a clinician.

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WOW, don't see anti-JK3 too often!

Have you already pursued family members and extended family members?  Also, is there a ethnic group you may want to screen?   We have had some success in the past in our area with Native Americans whom have had some members with a antibodies to a high antigens.

Certainly would want that patient and or other family members start donating and freezing their donations for their and others' future.

Technically, I agree with Mr. Needs approach with trying to resolve your immediate requirements.

Good luck and best wishes for your patient's recovery.

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I apologize for the delivery of my plea. The patient only has anti-Jk3, anti-E, and anti-c period.  The others listed is what he tests negative for regarding his antigen typing. Thank for for the quick responses, we will have a discussion with our pathologist and the patient's MD and decide from there. Malcolm I know you are retired but your expertise is welcome each and every time. I'm just wondering how to result our crossmatches. I guess we can result the units as "least incompatible" (because they are) and enter a comment on this sample such as " Phenotype matched (or identical) rbc's given for transfusion" ?? With phenotype identical blood that is incompatible, would the results of the bioassays, (MMA, ADCC ,CLT, IgG subtypes) possibly show that maybe he has an antibody to a low frequency antigen? Gee how 'unlucky' can this person be? I guess anything is possible. 

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9 hours ago, jojo808 said:

Patient has the following antibodies: (Pt is B+)

Jk3, E,c, He phenotypes K, Fya, S, N negative. Our ref lab found us 2 units that are phenotyped matched, one B+ and one O+ rbc. They are both incompatible, the O+ is 1+ in Gel, the B+ +/-.

Auto control Neg, DAT neg (reference lab results). What's our next step??? BTW hope you all are doing well during this time. 

This may be a little heretical, but I think I would avoid the gel test in this case. Perhaps do the cross-matching in a test system that's not as sensitive ? Local policy permitting, of course. A plain old tube test would probably result in compatible crossmatches.

The gel test system has probably not seen many cells with the Jk(a-b-) phenotype, and I also suspect that they're probably "sticky", especially if the cells have be frozen/deglycerolized.

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2 hours ago, exlimey said:

A plain old tube test would probably result in compatible cross-matches.

The gel test system has probably not seen many cells with the Jk(a-b-) phenotype, and I also suspect that they're probably "sticky", especially if the cells have be frozen/deglycerolized.

exlimey, I would most certainly agree with your first comment.  In the VERY old days, when I was merely middle aged, and we only had access to tube tests and reagents, including AHG, and techniques (such as tile techniques), we didn't kill patients by the thousand, so techniques that are a little less sensitive than are available these days, will not necessarily condemn the patient to a certain and painful death, despite the deafening shouts of those who are gainfully (and, in many cases, VERY gainfully) employed within the neo-science of quality for quality's sake (we needed to pull up our socks in terms of quality, but it has got out of hand).

On the other hand, having seen a fair smattering of Jk(a-b-) patients with anti-Jk3, I am unaware of "sticky" Jk(a-b-) red cells, even when they have been cryopreserved and reconstituted.  I am willing to, and will freely admit to being wrong, if I am proved so.

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14 hours ago, Malcolm Needs said:

exlimey, I would most certainly agree with your first comment.  In the VERY old days, when I was merely middle aged, and we only had access to tube tests and reagents, including AHG, and techniques (such as tile techniques), we didn't kill patients by the thousand, so techniques that are a little less sensitive than are available these days, will not necessarily condemn the patient to a certain and painful death, despite the deafening shouts of those who are gainfully (and, in many cases, VERY gainfully) employed within the neo-science of quality for quality's sake (we needed to pull up our socks in terms of quality, but it has got out of hand).

On the other hand, having seen a fair smattering of Jk(a-b-) patients with anti-Jk3, I am unaware of "sticky" Jk(a-b-) red cells, even when they have been cryopreserved and reconstituted.  I am willing to, and will freely admit to being wrong, if I am proved so.

I like your "neo-science" quote !:D

As the actual science has progressed, and the sensitivity of assays has increased, workers have encountered "-only" antibodies: albumin-only, enzyme-only, LISS-only, PEG-only, solid-phase-only, Gel-only. As you point out, if the older assays were that bad, we'd have patients dropping all over the place due to the presence of "missed" antibodies and false-negative crossmatches.

My point about the "stickiness" is that the gel system is notoriously unforgiving with anything but completely normal, healthy, well-washed cells, preferably in the manufacturer's diluent. Throw anything at it that's little different and you risk incomplete or unsatisfactory centrifugation of red cells. I don't know if that specifically happens with Jk(a-b-) cells, but I have seen frozen/thawed cells behave badly.

After reviewing the posts here , I think it's perhaps a little more worrying that jojo808's group may consider transfusion of "least-incompatible". I understand that needs must, but that's a dangerous proposition if one doesn't know the specificity of the antibody(ies) causing the incompatibility.

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2 hours ago, exlimey said:

After reviewing the posts here , I think it's perhaps a little more worrying that jojo808's group may consider transfusion of "least-incompatible". I understand that needs must, but that's a dangerous proposition if one doesn't know the specificity of the antibody(ies) causing the incompatibility.

I couldn't agree more.  That's why I mentioned so many caveats.

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So we did perform the tried and true tube method with Peg enhancement (actually our secondary method) and both units came out a clean negative. The MD wanted to transfuse only one unit and see how the patient does. I'm so ok with doing that. I will try and keep you all posted thank you all again. 

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On 4/29/2020 at 12:14 PM, mrmic said:

WOW, don't see anti-JK3 too often!

Have you already pursued family members and extended family members?  Also, is there a ethnic group you may want to screen?   We have had some success in the past in our area with Native Americans whom have had some members with a antibodies to a high antigens.

Certainly would want that patient and or other family members start donating and freezing their donations for their and others' future.

Technically, I agree with Mr. Needs approach with trying to resolve your immediate requirements.

Good luck and best wishes for your patient's recovery.

Polynesians/Pacific Islanders.

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27 minutes ago, Baby Banker said:

Polynesians/Pacific Islanders.

True, but if you read page 660 of Issitt PD, Anstee DJ.  Applied Blood Group Serology.  4th edition, 1998, Montgomery Scientific Publications, you will see that the percentage of Jk(a-b-) individuals was very much over-estimated in the original paper.

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On 4/29/2020 at 12:14 PM, mrmic said:

WOW, don't see anti-JK3 too often!

Have you already pursued family members and extended family members?  Also, is there a ethnic group you may want to screen?   We have had some success in the past in our area with Native Americans whom have had some members with a antibodies to a high antigens.

Certainly would want that patient and or other family members start donating and freezing their donations for their and others' future.

Technically, I agree with Mr. Needs approach with trying to resolve your immediate requirements.

Good luck and best wishes for your patient's recovery.

Polynesians/Pacific Islanders.

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We had a patient with anti-Jk3.  We were able to find units for him once the blood supplier started looking at Polynesians and Pacific Islanders.  

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Fast forward: We think the cause of the incompatibility was (maybe) an Anti-Lea. We came to this conclusion because the 2 units that were clean were LeA negative and the other 2 that were reactive with the patient's plasma were LeA positive. This would be the only antigen that did not match the patient's phenotype. Anyway we are hoping our blood supplier can continue to get these (few) donors in. I think I've read in the past where anti-LeA is not clinically significant, but if this is an anti-LeA, it is not being detected by our ref lab who uses solid phase and tube. We use Ortho Gel (we do not have automation yet), soon to get the Biorad IH 500. Can't wait with all our antibodies!

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Anti-Lea CAN be clinically significant, but it is very rare for it to so be, and it tends to be self-limiting.  For it to be clinically significant it has to be IgG and/or complement activating, and it is self limiting because, of course, the Lewis antigens are soluble.  This means that they will be in any plasma remaining on the red cells in the unit, and these soluble antigens will inhibit the patient's anti-Lea in vivo.  You can usually continue to transfuse the same unit that caused the problem after a while, with no further problems.  MIND YOU, you have to be ABSOLUTELY CERTAIN that it was anti-Lea that caused the reaction in the first place!

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When you say that the antigens are soluble and will inhibit the patient's anti-Lea in vivo, does that mean there will eventually be no Lea antigen on the donor rbc's? And let's just say it is certain that this patient has anti-Lea. Would there (theoretically) be no further problems with the first unit? or subsequent units? 

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Yes, the transfused red cells would eventually become the same Lewis type as the recipient.  This has been known for some time, see Sneath JS, Sneath PHA.  Adsorption of blood-group substances from serum on to red cells.  Brit med Bull 1959; 15: 154-157, and Needs ME, McCarthy DM, Barratt AJ.  ABH and Lewis antigen and antibody expression after bone marrow transplantation.  Acta Haemat 1987; 78: 13-16.

Not only in theory would there be no problems giving the rest of the first unit (as long as it is given relatively quickly after the first few mL, but it has been shown to be safe in practice.  However, of course, the immune system will continue to produce anti-Lea, and so this "protection" will only last for a finite time.

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