Leaderboard

I did allo-adsorptions on eluates for quite a while and never once detected anything in the adsorbed eluate. My own experience suggests that it is a waste of time and resources, but others may disagree.

I do not have any remote refrigerators but, is there a way to have an automated comment added to the unit history when a unit is removed from the remote refrigerator that states it was visually inspected? That would give you documentation. Of course, you would need to have clearly stated in your policy that visual inspection is performed when units are retrieved, and nursing training would have to have that documented as well. That's how I would resolve that issue. That said, I think that the inspector may be improperly applying the checklist item to your situation. The checklist item states: TRM.40900 Blood/Tissue Sign-Out Phase II The process for signing blood and tissue out of the laboratory provides adequate protection for the potential recipient. NOTE: A person authorized by the transfusion medicine service must perform a clerical and visual inspection of each component immediately before it is issued. Transporters of blood components and tissue must be trained in prompt delivery. Training may consist of instruction at the time the product is dispensed. There is no blood bank staff that is "issuing" the blood so, technically, there is no "person" signing out the unit. I would argue that the inspection would have to take place when the unit is placed in the remote remote refrigerator. I would challenge the deficiency on those grounds.

I agree with Malcom - not much value, if any. I, too, have done many such noninformative adsorptions. In a recently-transfused patient, there is perhaps a very remote chance that (allo)adsorptions on an eluate would reveal a "only on the cells, not in the serum yet" newly formed antibody. This might be important if the clinicians suspect faster-than-normal red cell loss, but it would be very difficult to differentiate from the typical increased red cell demise seen in patients with warm autoantibodies.

I have an idea of what I think it might be, but I would hesitate to say without a bit more information concerning the condition and underlying pathology of the patient. How old is the patient? Have they recently had something like an atypical pneumonia? I think, without knowing the answer to the above questions, that the specificity of the antibody MAY be between "anti-O" and "anti-Q". I would suggest performing an indirect DL-test. I may well be wrong, OF COURSE, but the attached may help. Paroxysmal Cold Haemoglobinuria (PCH).pptx

I was joking about the specificity being between "anti-O" and "anti-Q", in that anti-P, the specificity almost always involved in a case of PCH is a "cold-reacting" IgG anti-P that "fixes" complement (and P is between "O" and "Q" in the Western alphabet). A pretty poor attempt at a joke, I fully admit! While I am not saying definitely that it is a case of PCH, the fact that the patient has a suspected AIHA, that the auto-antibody appears to be "cold-reacting", that it is IgG and that it also involves activated complement, strongly suggests that this may be the line to go down as an investigation. We didn't perform a DL test routinely by any manner of means (despite being a London based Red Cell Immunohaematology Laboratory). It was always discussed between our own Consultant (or, at night, weekends or Bank Holidays) by the on-call Consultant, but all of the staff knew how to perform the test, even if they were a lone worker. We always used to dread being asked to perform such a test as a lone worker, as it took so long to do!

Here are our "nudge" questions. See my other post for our rounds etc.

We created a policy to ask at certain stages whether the MTP is likely to go on at the same rate so we can plan for blood ordering since we are several hours' drive from our supplier. We have this on the back of our MTP log sheet: "Assess Futility? Round 10 cooler has left BB within the first 3 hours of MTP (or inadequate blood supply): • Evidence shows a much-reduced chance of survival if over 40-50 RBCs have been transfused in an MTP. • Pathologist can confer with providers regarding the chance of saving the patient with continued transfusion. • Be prepared to provide pathologist with available blood supply information and expected arrival of more units" Our rounds contain 4 RBC units plus varying yellow stuff. We are starting the conversation at about 40 RBCs, so we have an answer by 50, we hope. We don't have other hospitals nearby that we can borrow more than a few units from.

No AABB standard requires a crash cart. Donors do not develop anaphylactic reactions, but this type of reaction is why offices or facilities that administer transfusions or IVIgG (and similar products) need to be able to administer epinephrine emergently. Most of the rest of the stuff in a crash cart would never be needed and certainly not for blood donors. So no crash cart unless you are administering human blood products or drugs that can cause anaphylaxis.

I would make the argument that the blood was inspected when it was issued to the remote storage unit. At that point the transfusion service had completed it's obligation. I am assuming (and we all know how that goes!) that the remoted storage unit has been exhaustively validated and monitored with documentation to confirm my assumption. As well as any training required for those accessing the remote storage unit. I'm always more worried about the blood going to the wrong patient in these situations than I am for the quality of the unit. Personally I always enjoyed challenging such citations.

That's still a significant number of A subgroup kidneys to give B patients. Patients who are type B and need a kidney transplant usually have to wait years, and sometimes die because no type B kidney is available.

How do you get hold of the extremely rare antibody specificities I mentioned (such as anti-Vel) to regroup units sent from, possibly, frozen blood banks, that they have typed as Vel Negative before the unit is sent out?

"The bottom line was, if the treating physician wanted to use up the entire inventory trying to save a life, we could not deny them the blood, even though it places other patients at risk. " I would call this some combination of cowardice and insanity, speaking purely personally. Taking responsibility for difficult decisions is why physicians get paid well, and avoiding decision making is irresponsible.

Man you got me good, started searching for anti-O and anti-Q and thought that I missed something big It's cool, no hard feelings! Anti-P sounds much more familiar. That's why we don't do DL test ourselves, we don't have time for it.

I would add it to the title. For instance, I my blood bank collected donors, provided blood for transfusion, and participated in stem cell collection and infusion, my department would be called, "Transfusion Medicine, Donor Services, and Cell Therapy Laboratory."

I suggest reaching out to your director of the O.R. and to your Biomed Director. Start a conversation with them showing them the CAP standard and ask them how they are measuring the safety and efficacy of recovered products. Ask them to provide you a copy of their data to include in your records. Also, since your medical director has to actively participate in the program, they may need to officially report to them as well. Perhaps this could be covered in your transfusion committee, if you have one.

We normally used a ratio of 1:1, unless the antibody was particularly weak, in which case we would, on occasions, go up to 4 of plasma/serum to 1 of red cells in NISS (BUT, make sure that such a ratio is written into your SOP).

This is fascinating stuff. A lot of science, learned the very hard way, with a heavy dose of art. I don't envy those having to make these calls.

I don't know what the titer is for incompatible kidney transplant, but for hearts they prefer less than 1:4, but there are other criteria as well. If the patient is less than 12 months old, they don't worry as much about the titer. I think they won't consider a patient who is over 2 years old. Again though, that is for hearts.

"Just curious, can one give a group A1 kidney to a group B patient who has a very low isoagglutinin titer ?" It's been done. Depends on the ability to suppress the anti-A titer low enough through immunosuppressive drugs and plasma exchange, the usual preparative regimen. Obviously ABO identical is best, but this is an alternative at some centers with experience doing these transplants.

Somewhere, in Patrick Mollison's work, cited in Blood Transfusion in Clinical Medicine, he mentions that IgG ABO antibodies are more clinically significant in solid organ transplants than are IgM (if I remember correctly, he specifically mentioned renal transplants), but I cannot cite the exact paper off the top of my head (I will see if I can find the reference). As a result, whenever we were dealing with a renal transplant that crosses the ABO barrier, we almost performed an IgM and an a separate IgG titre. Whether this is now considered to be necessary, I will leave to other people to discuss!

PathLabTalk would like to wish all members celebrating their birthday today a happy birthday. Makana (67)itslallu (41)echubar (54)John McKamely (46)abdulfattah (44)bgend (62)Kifayat Mufti (36)CSP0102 (64)lilly (47)j.ulrich (40)bmanski22 (37)

I second the Echo suggestion. I have had zero issues getting reagents through the whole Covid/supply chain problem period (which is ongoing). We are geographically isolated customers but still receive good support service when we need it. Pricing for tube reagents is much cheaper when your facility is in the automation pricing tier.

The policy at all places I have worked; to find antigen negative units in our inventory requires testing two different segments sequentially (not parallel). First segment is a screen and second is confirmation.

Thanks ELondon. Could I just say again, even if the Reference Laboratory does detect an antibody (or more than one, come to that), it is not a particularly abnormal thing in pregnancy, but it does not mean for one minute that the pregnancy will be affected; Mother Nature has seen to that. There is another Blood Group System named Lewis. The antigens within this system are soluble in the plasma part of your blood, and are adsorbed onto the red cells from the plasma (they are not intrinsic to the red cell membrane). During pregnancy, the concentration of plasma lipoproteins (fatty proteins in the plasma) can increase enormously (about four-fold). These plasma lipoproteins "mop up" the soluble Lewis antigens, and a pregnant woman, who would normally be, for example, Le(a-b+), can become Le(a-b-), and may even, temporarily, produce antibodies against the Lewis antigens (an individual hardly ever produces antibodies against an antigen that they express - but strange things happen in pregnancy!). In addition, ALL babies are born as Le(a-b-), so any Lewis antigens Mum produces will NOT affect the baby! There are many, many other antibody specificities that will not affect the pregnancy at all. Now, I should say two things. Firstly, I cannot say, from a distance, what is the antibody in your plasma (that can only be done by the laboratories at the Hospital and the Reference Laboratory, but it does not sound at all serious). Secondly, i am what is called a Biomedical Scientist, not a doctor, and so I am, by Law, not allowed to diagnose (as far as I know, neither is the midwife), and this is why I am so glad that you are going to see an Obstetrician, who, I hope, will be able to reassure you even more. Mean while, sleep easier, and enjoy your pregnancy!

PLEASE do not worry. Your midwife is COMPLETELY wrong, and really should not comment about something she patently does NOT understand, and about which she has a pitiful amount of knowledge. She should never have answered your questions with her lack of knowledge, but should have left it to your Obstetrician. I note that you are a fellow "Brit"! Within the British population, the percentage of people who have the R1R1 type (which is a type within the Rh Blood Group System) is 16%. Also within the British population, the K- type (which is part of the Kell Blood Group System) is 91%. What that means is that 91% of 16% of the British population is R1R1, K-, or, give or take, a few decimal points, 15% of the British population (about an eighth of the British population). On Friday, 19th October 2018, the British population was measured as 66,690,116! Let's call that 16.5 million in round numbers. This means that, give or take, 9, 975, 000 in Britain are R1R1, K-. Now, admittedly, your midwife will only be looking after women, but, even then, that means 4, 987, 500 women will have the same Rh type and K type as you! How your midwife has only come across your "rare" type four other times in her career, is beyond belief (and I genuinely mean BEYOND belief), unless, as I say, her knowledge of blood groups and blood group serology is incredibly poor, and I repeat, she should NEVER have worried you like this. Just in case you think that I do not know what I am talking about, I have worked in the field of blood transfusion/blood group serology for 43 years, have been an internationally invited lecturer and am the Chief Examiner in Transfusion Science for the Institute of Biomedical Science in the UK, and am a co-author of the British Society of Haematology's Guidelines for Blood Grouping and Antibody Testing in Pregnancy. I don't write that to "blow my own trumpet", as it were, but to try to reassure you that I actually do know what I am talking about. I should warn you that "consulting Dr Google" is equally as useless as listening to your midwife. You should really relax. YES, it is possible for you to produce red cell antibodies during your first pregnancy, but it is INCREDIBLY RARE. It is even more rare for such an antibody to cause any problems in a first pregnancy. I notice that the report from the Blood Bank was that they detected WEAK reactions with 26 of 30 panel cells, but they could not identify a specificity. They have requested three further samples of blood to send to the Reference Laboratory. Again, to give you some comfort, I hope, I ran a Reference Laboratory in London for 16 years before I retired in 2016, and we saw, quite literally hundreds of cases like yours. For a red cell antibody to cause any problems within you pregnancy, it would have to have a titre of 32 or above (this means that it would still be detectable when it has been diluted THIRTY TWO times). I can assure you that the mere fact that the Blood Bank reports weak reactions means that there is ZERO chance that the titre will be 32 or above. If a Hospital Blood Bank, however big or famous the hospital may be, cannot identify an antibody, it is almost universal practice that samples will be sent to a Reference Laboratory for further testing - AGAIN, DO NOT WORRY ABOUT THIS. There are many, many red cell antibodies that are clinically insignificant, both in terms of transfusion reactions and haemolytic disease of the foetus and newborn (which is what your midwife has left you worried about). I KNOW it is difficult, but PLEASE do not worry. PLEASE take no notice whatsoever of your midwife on this matter (I am sure she is an excellent midwife, but she is patently no expert in the field of blood groups), but DO talk to your Obstetrician, who, I hope, will have talked to your hospital's Haematology Consultant, who, in turn, will have spoken to the Consultant in Charge of the Reference Laboratory, and I am sure that they will echo my opinion that there is NOTHING to worry about. Oh, and lastly, I am R1R1, K- myself!!!!!!!!!!!!!

@Malcolm Needs......YAY! it always makes me feel a little "smarter" when my thoughts are consistent with your answers!!! PCH was my first thought!

First, blood given pre-hospital is quite routine these days. Both ambulances and helicopters are carrying Low Titer O Positive whole blood that they transfuse on scene in response to traumas and hemorrhagic shock. In South Texas, the ambulances and helicopters receive their blood directly from our blood supplier. Who will be stocking your helicopter? Will it be your facility? If so, you have a lot of work to do. If your supplier, you have nothing to fear. Second, when a unit is given pre-hospital, our EMS techs give the empty blood bag and a record of transfusion to the receiving nurse in the Emergency room, who then sends them to the blood bank (theoretically, practically we seldom get them right away). Our emergency room physician orders a type and screen upon arrival. Only if an antibody is detected (or we have a history of a clinically significant antibody) will we perform any crossmatching with the unit. I would suggest you google the topic Low Titer Whole Blood. It will help you answer your question.

When you use extended sample expiration, how does this affect electronic crossmatch? The sample collection date would cause our LIS to reject the EXM rule. Do you just perform IS serological crossmatches?

We do 21 days.

Transfusion Medicine in our institution includes the Blood Bank/Transfusion Service, Donor Service and Stem Cell Processing Laboratory. Outside each facility we have the relevant signage. Some places it includes Therapeutic Apheresis, which in our institution is both physically separate (so is our Donor Room) and located in the Dept. of Medicine (Cancer Center). As long as the facilities are well defined, I'm not sure the overall name matters much, except on stationery, which no one uses much anyway :).

We do up to 30 (33 actually) days. If sample collected 1/21/23 and surgery is 2/21/23 - we set exp of sample to 2/21/23. On DOS if all documentation is rec'd from OR - then extend 3 more days.

We extend for 14 days.

Part time / guest lecturer at your nearest Med Tech school?

Thanks. Probably an unanswerable question: How low a titer is "low enough" ? A follow-up.....can one transplant an A1 kidney into an A2 patient with anti-A1 ?

Apologies in advance for my ignorance on these matters. Are the units/products in the remote storage locations assigned to specific patients, or are they available to random patients ? If the former is true, arguably they've already been issued.

Our Blood Bank performs A1 lectin testing of the potential A donor. If they are positive, they are eliminated as a donor. as for the recipient - all B patients (potential mis-match recipients) are titered against an A subgroup cell (A2 reagent red cells here) to determine their antibody reactivity. The clinicians have an established threshold for a suitable titer (which I do not know) Potential B recipients who have an Anti-A titer with A subgroup cells below the established threshold could potentially receive an A subgroup kidney. As for O recipients - we make our own 0.01MDTT treat their plasma to determine IgG vs IgM antibody reactivity titers.

Our facility has recently switched to Grifols and we are very pleased. We have an Erytra Eflexis and have not had any supply issues. The customer service has been great and they are very responsive to all of our questions/concerns.

Been using the Grifols Erytra for a few years and I'm a big fan. I find it very user friendly and efficient, low maintenance and none of the garbage reactions I've had to deal with before with Echo and Ortho The only supply chain issues I have had were FedEx related and my rep has always been fantastic communicating any issues and ensuring we got what we needed.

We currently use the blood admin snapshot and BPAM. I'm curious to if we can include it in the MAR medication admin module. That's the screen nurses use most and blood admin would fit will within it. It's a scrolling timeline that is visually very user friendly. I just don't know if that information is something someone in Lab (me) can see for transfusion information. My problem with the snapshot is that with it being something rarely used for most nursing units, completion audits are awful. I've even found a unit left in "currently transfusing" status for over 48 hrs.

I would consider switching to Immuco ECHO Lumena before going to Grifols. You could also look at Bio-Rad's IH system for gel alternatives. That said, I prefer Ortho for gel and Immucor for solid phase.

In our case it would be not totally trusting your own work and asking a second tech to double check with a new segment.

To quote my first BB manager “first rule of BB; get the ABO right, last rule of BB; get the ABO right. “

If you are screening unknown units in your inventory then a second confirmatory test on that unit is strongly advised. If you receive labeled antigen negative units from your reference lab then believe their process and the label. Retesting because a tech does not trust someone else’s work due to “comfort” seems to be a waste of time and money.

We don't recheck antigen typings here in our hospital in Canada. The typings that have been performed at Canadian Blood Services, are embedded in the barcode on the bag, with all negatives printed on the End User Label. Every unit is antigen typed for K so if it isn't printed on the bag the unit is K Pos. Antigen typings we do are all linked to the unit through barcode. The reason of, "We were typing a lot of units and may have mixed them up", is not acceptable in a blood bank setting. Go work in a different department if you can't organize yourself. Anyway, there is also a full gel or whatever you use crossmatch at the end of that phenotyping, as long as the antibody is reacting, an anomaly could be discovered there. You have to have a little faith that people before you are doing their job properly, or you can cause yourself a lot of undue stress.

There are no data suggesting a particular limit. Survival is very unusual after 30-50 units of red cells, but everyone has exceptional cases like those mentioned above. We have discussed futility of care many times, and our practitioners are quite amenable and forthcoming. We have stopped resuscitation in a young man having a liver transplant go badly, when there was no surgical path to hemostasis after about 250 units, but this is unusual too. Bottom line, a case by case decision as to whether care is futile and/or the patient's needs endanger the well being of other patients needing transfusion. Those are the key issues in each case to my way of thinking.

There is reason NOT to use the freshest possible units. They may be more toxic than intermediate stored units. This is something that made sense but was almost certainly wrong. See below for the reasoning and published data. We use <21 days as fresh for this reason and avoid <7 days storage for everyone based upon the randomized trial data. BMJ 2019;366:l4968 doi: 10.1136/bmj.l4968 (Published 5 August 2019) Page 1 of 1 Letters Trivella and colleagues present some caveats around the subject of duration of red cell storage and clinical outcomes.1 Studies have been widely interpreted as showing that transfusion is not associated with adverse clinical outcomes. I think this is a serious misinterpretation of the data. In addition to the concerns raised by the authors, another valid hypothesis, which has received little attention, is that very short storage red cells might be more dangerous than medium storage periods (say 7-21 days) and equally dangerous as longer storage red cells (say 28-42 days). An inverted U shaped curve. The evidence for this comes from a meta-analysis finding that “ultra short” storage of red cells was associated with a post-transfusion increase in nosocomial infection.2 Shorter storage red cells have a greater imbalance of oxidation-reduction potential than longer storage red cells in preliminary studies in vitro.3 Red cell storage duration is also a poor predictor of post-transfusion free haemoglobin and heme, putative mediators of toxicity from transfusions.4 5 We need better metrics for predicting red cell transfusion efficacy and toxicity. The simple expedient of fresher red cells is clearly not that metric and might be leading us to transfuse more toxic red cells (very fresh) in the most fragile patients, such as premature newborns. A new approach is clearly called for by the current data. At our centre we define fresh as <21 days of storage, and we generally never transfuse a red cell that has been stored for much less than 7-10 days, for the above reasons as well as logistics of supply. Competing interests: None declared. 1 Trivella M, Stanworth SJ, Brunskill S, Dutton P, Altman DG. Can we be certain that storage duration of transfused red blood cells does not affect patient outcomes?BMJ 2019;365:l2320. 10.1136/bmj.l2320 31186250 2 Alexander PE, Barty R, Fei Y, etal . Transfusion of fresher vs older red blood cells in hospitalized patients: a systematic review and meta-analysis. Blood 2016;127:400-10. 10.1182/blood-2015-09-670950 26626995 3 Schmidt A, Gore E, Cholette JM, etal . Oxidation reduction potential (ORP) is predictive of complications following cardiac surgery in pediatric patients[abstract]. Transfusion 2016;56(Supplement S4):20A-1A. 4 Cholette JM, Pietropaoli AP, Henrichs KF, etal . Elevated free hemoglobin and decreased haptoglobin levels are associated with adverse clinical outcomes, unfavorable physiologic measures, and altered inflammatory markers in pediatric cardiac surgery patients. Transfusion 2018;58:1631-9. 10.1111/trf.14601 29603246 5 Pietropaoli AP, Henrichs KF, Cholette JM, etal . Total plasma heme concentration increases after red blood cell transfusion and predicts mortality in critically ill medical patients. Transfusion 2019;59:2007-15. 10.1111/trf.15218 30811035 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/ permissions LETTERS

I'm sorry, but I find this appalling. Fancy worrying you like that. I know that I said only 5 people per 1, 000 are Co(a-), but in 2014 (the last year to which I have access, as I am retired) NHSBT had 38 such units frozen down in the National Frozen Blood Bank, and well over 100 "walking donors", who we could call upon at any time, to provide "fresh, liquid" blood. If you compare the number of people living in the UK (and the size of the UK come to that) to the number of people living in the USA (and the size of the USA, where many of the individual states on their own are larger than the UK), you can see that the USA would also have had numerous compatible units frozen down, and would also have had many, many "walking donors". It is totally unacceptable that the medical staff should have frightened you like that, with comments that are patently untrue.

Quick update on my case: I submitted a further blood test, as requested by the lab. Received the results nearly 3 weeks later. Turns out that no alloantibodies were identified in the samples. The comment from the lab says: 'One reaction of no apparent specificity was detected by the following techniques Bio-Rad IAT. No alloantibodies were identified by the following techniques: Bio-Rad Enzyme IAT BioVue IAT. Antibody and clinical significance: This antibody is unlikely to cause haemolytic disease of the fetus and newborn. Repeat sampling: No further samples are required for reassessment in this pregnancy. So it looks like the initial test, that I was so worried about, was a 'False positive' so all good in the end. Most grateful for Malcolm's helpful responses, I did learn a lot in the process.

The first thing to say is that almost everyone is that, roughly speaking 98% of all the people within the White populations are Kp(a-), and, as near as makes no difference, 100% of the Black populations are Kp(a-), so this part of your group is not only normal, but very normal indeed. The part of your group that is rare is the fact that you are Co(a-). Only approximately 5 people per 1, 000 are Co(a-), so the chances are that your partner is also Kp(a-), but would be Co(a+). This means that your daughters are very likely to be Kp(a-) and Co(a+b+), getting their Co(a+) from your partner, and their Co(b+) from you. All that having been said, only the genes governing the red cell groups are inherited from their parents. Do I take it, from your chosen name, that you have an anti-Kpa and/or an anti-Coa? If so, do not worry for a single second. Your daughters will not inherit your antibodies, and it is these that cause problems and complications in pregnancy. For your daughters to have complications in pregnancy, they would have to be exposed to Kp(a+) blood, either from a transfusion, or by a previous pregnancy (their previous pregnancy, not yours). As I said above, the chances of their partner being Kp(a+) is only 2%, and even then, it has to be remembered that not everyone who is Kp(a-) and is exposed to the Kp(a) blood group make an anti-Kpa. Even if they do make an anti-Kpa, it is incredibly rare for anti-Kpa to cause any problems in pregnancy. In the case of the Colton blood group (the Co bit), as all of your daughters are likely to be Co(a+b+), and it is not usual by any means for people to make antibodies against a blood group they express, it is even less likely that any pregnancy will be complicated by anti-Coa. I'm not sure how well I have explained all that, but I really don't think that either you, or your daughters, have anything to worry about concerning problems with pregnancy as a result of your blood type.

I'm afraid my answer this time is going to be less helpful, because it very much depends upon the particular technology used by the laboratory, meaning that there is no single answer (and 28 weeks of pregnancy, from this point-of-view, is irrelevant - we would do the same tests at any stage during the pregnancy). The majority of hospital laboratories use a technology known as column agglutination technology, or CAT. With this, the reactants (for example, your plasma and a sample of donor red cells) are pipetted into what is known as a "reaction chamber" at the top of the column, after which the whole thing is incubated at 37oC (body temperature) for about 15 minutes, and the card is then centrifuged at a specific speed for a specific time (there is a bit more to it than that, but I don't want to go into too much detail and confuse the issue). This type of technology is superb for detecting clinically significant antibodies, but can be prone to detect clinically insignificant "cold-reacting" antibodies, that will cause neither a transfusion reaction, nor problems with a pregnancy (haemolytic disease of the foetus and newborn). These are sometimes called "false positives", although, strictly speaking, they are true positives, but not really the type of antibody we want to detect. This is a bit of a nuisance (for us). There are loads of other technologies and techniques, but the Reference Laboratories will have access to almost all of these. In addition, the Reference Laboratories will have access to many more examples of rare red cells and grouping reagents. In a case like yours, I would think that the Reference Laboratory would first work out the actual specificity of your antibody, and then perform tests (probably in good, old-fashioned test tubes) to see whether the antibody reacts at 37oC or at a lower temperature. This will tell them whether or not your antibody will need to be monitored throughout your pregnancy. I would be very surprised, given what you have told us about your case, if the Reference Laboratory would require another sample during your pregnancy, as 28 weeks of pregnancy is thought of as a sort of "cut off" point - BUT, I must reiterate, I am commenting "from afar", for one thing, and, in any case, am not allowed to diagnose or give specific advice to your case.