johna
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Posts posted by johna
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Invariably we are finding that reactions with anti-D in gel as high as 2+ turn out to be <1+ in the first tube when a saline tube titer is performed. Is anyone else experiencing this? If so, would you consider it a waste of time to titer 2+ anti-D gel reactions?
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We generally go to a PEG panel which includes an immediate spin (before adding PEG of course). If the PEG panel is negative and the MTS result doesn't make any sense I wouldn't have any problem defaulting to the PEG results.
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My quandry is....do I do a titer for pregnant patients if the antibody is non-reactive in AHG at 37C? The old wisdom says no titer, but this article makes me uneasy. On the one hand, I hate to rack up big bills for these patients. On the other hand, maybe the (ultra) conservative course of doing the titer is best.
I'm not sure what good a Coombs titer would do if the antibody is not active at 37C; unless of course you are referring to a room temp titer. In that case I think you would be creating a lot of patient/physician anxiety for no reason.
This whole situation reminds me of the days of using enzyme-treated screening cells to
detect anti-JkA/B. Might you miss a Kidd antibody without using these cells? Sure! But is it worth the time, expense and frustration dealing with treated cells to pick up the rare enzyme-only antibody? I think most of us would say, "No!"!
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Ok, I figured it out:
Fetal hemolytic anemia and intrauterine death caused by anti-M immunization
Transfusion
Volume 47, Issue 5, Date: May 2007, Pages: 911-917
Agneta Wikman, Ann Edner, Gunilla Gryfelt, Baldvin Jonsson, Jan-Inge Henter
STUDY DESIGN AND METHODS:This study reports on three pregnancies in one family that all resulted in severe fetal anemia. The first fetus died in utero with hydrops fetalis during the 20th gestational week and the second child was delivered after 28 weeks of gestation with hydrops fetalis and a hemoglobin level of 16 g per L whereas the third affected child was treated with intrauterine red cell (RBC) transfusions before delivery at 28 weeks of gestation.
RESULTS:The direct antiglobulin test was negative but anti-M in a low titer was detected through the three pregnancies, and its clinical relevance, which initially was uncertain, was confirmed by pronounced in vivo hemolysis in maternal blood of chromate (51Cr)-labeled M+ RBCs and normal survival of 51Cr labeled M– RBCs.
CONCLUSION:It is concluded that anti-M immunization in a few cases may cause severe fetal hemolytic anemia and intrauterine death. It remains to be elucidated why a normally clinically insignificant antibody is this aggressive in a small proportion of cases. Because the condition is treatable, anti-M must be considered as a possible cause of fetal anemia and intrauterine death.
Thanks for the followup Linda. Somehow I definitely missed this article.
I'm not sure whether an isolated case like this this should change the way we look at an IgM anti-M. For several years our reference lab has run into a few of these on a daily basis and we have never had a response from a client indicating a problem at delivery. Was wondering if anyone on the board has experienced or become aware of a similar problem.
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I would suggest investigating pricing from Alba Bioscience in Raleigh, NC and Biotest in Denville, NJ. These two companies are new to the BB marketplace but may have decent pricing for non-gel & non-solid-phase reagents.
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As I'm sure the folks that frequent this forum are aware an Rh control is necessary if the patient types as AB+. Personally I've always found it easier to routinely run a 6% albumin control instead of backing up and pulling all the AB+ specimens out of a run. I think that the fact that an in-house prepared Rh control does not contain preservatives or antibiotics is really not an issue. Just an opinion!
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Was wondering how folks who are performing titers in gel have handled the situation of indicating to the docs what titer values should be considered a cause for possible intervention. The ACOG bulletin concerning Management Of Isoimmunization in Pregnancy indicates that a Coombs titer of 32 be considered significant in this respect. The bulletin does not mention any specific antibodies but I believe this would apply only to Rh. In light of the higher gel titers would you now be telling the OBs that 128 is the new baseline?
Has anyone evaluated gel titers and made the decision to stay with tube? Thanks!
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John,
Of course we back up a report of passive anti-D by investigating whether the patient actually got ante-partum RhIG at another facility, if not in our records.
As far as the baby's results, even if the baby's DAT is positive and you elute anti-D, the doctor won't care as long as the bilirubin stays low.
We had a mother with an anti-D with a titer of 256, and an anti-C with a titer of 128. Both antibodies were eluted from the baby's cells. The baby's first total bilirubin was 3.2. The next day 6.5, the day after 14.9. Then it started going down and the baby was discharged.
Gil
Thanks for the response Gil. Unfortunately as a reference lab we are privy to zero patient history information. If we called every client who sent us a weak anti-D we'd have to hire an FTE just for phone calls.
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Page 548 of the Technical Manual gives a very inexact method of postulating whether the anti-D is active or passive and how often are any of us encountering an IgM-only anti-D to indicate active immunization. If the antibody reacts at room temp and in the Coombs phase I would seriously doubt the chances of 2ME or DTT solving the problem.
We deal almost exclusively with a prenatal population and if the intial screen is positive by solid-phase and the antibody is identified as anti-D a tube screen that gives a reaction of less than a good 1+ is resulted with a "too weak to titer" comment. We still have docs calling up asking for an exact titer.
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I believe Ortho makes an Anti-C3d reagent and an Anti-C3b,-C3d reagent, but not an Anti-C3b reagent. A reagent that just contained anti-C3b would be of limited use (just IATs), it shouldn't be used as the sole reagent in DAT to detect complement (C3d and/ or C3b) on the patient's RBCs.
Thanks for the correction Kathleen, my miscue. You are correct. I should have said that Ortho makes an anti-C3d (not anti-Cb).
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I've posted a similar question regarding this on the AABB website but I'm hoping to cover all bases to get some feedback.
We recently encountered a high-titered anti-M and treated the serum with DTT. The saline control Coombs titer was 128 and the DTT-treated serum titer was zero. Now it seems to me that some time ago I saw a paper detailing a case in which an IgM anti-M had been implicated in HDN. Does anyone recall something like this?
Is anyone using DTT or 2ME in cases like this? We have recommended that the doc followup with DTT testing every 3-4 weeks. Thanks!
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I thought that Immucor had an Anti-C3b antisera also.
According to my product catalog they do not have an anti-C3b reagent.
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First of all Happy New Year to everyone!
As far as I know Ortho is the only company manufacturing an Anti-C3b product in the U.S. and they are also producing an Anti-C3b/C3d reagent. Was wondering if anyone has a preference between these two reagents and if so why? I believe there may be some price difference between the two which may be a consideration. Thanks!
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-----------------------------------------------------I don't see what the point would be. If you are looking for antigen-negative units and the donor result was antigen-positive you would exclude the donor anyway.
Correction on my previous post. After thinking about this for a while I've come to the conclusion that a DAT would be appropriate since you would want to label these units as antigen-positive, (even though you wouldn't be using them for the patient being crossmatched) and would want to ensure that the results were correct. I've been away from the hospital blood bank side of things too long!
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There are isolated reports of anti-E and anti-K being missed using a gel antibody screen and I believe that Ortho made a few adjustments in the product a while back which may have solved the problem. Has anyone encountered this problem recently?
Regarding gel titers. Rh antibody titers in gel appear to be significantly enhanced vs. tube testing. Has anyone seen this enhancement with other antibodies (K, FyA, etc.)?
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When you are phenotyping DONOR UNITS, do you do a DAT on all positive results to prove that the result is due to the presence of antigen on the cell and not because the unit has a positive DAT? I understand the need for this on a patient but question the need to do it on a donor unit.
I don't see what the point would be. If you are looking for antigen-negative units and the donor result was antigen-positive you would exclude the donor anyway.
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Food for thought!
The CAP Transfusion Medicine checklist TRM.32250 indicates that patient records should be retained for 10 years. Are not these antigrams considered "patient records"? What else would they be? The only mention of a 5 year retention period concerns quality control and retyping of donor unit records.
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I think this would be a very curious result. The gel technique is extremely sensitive and will pick up the majority of weak Ds (European box inserts state that anything less than a 3+ to be considered as a weak D) However, in my experience, testing of samples with a result of 1+ or 2+ with a weak D confirmation test (by IAT) is invariably stronger than the result in gel when I use our weak D confirmation reagent (exception - DIV is negative - but these give 4+ reactions with the ordinary Ds anyway).
It has turned unseasonably COLD here - -1° already. December weather!! Please send over some sunshine!!:cool:
I would have to agree with you Galvania. Weak D reactions by IAT with rare exception turn out to be stronger than gel reactivity.
On a side note, those of us in the Southeastern U.S. suffering from drought conditions would be more than willing to exchange some sunshine for a few days of rain.
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Here is the scenario:
Pt. red cells reacted 1+ immediate spin with monoclonal anti-D by two different labs, no weak D test performed. Reported as "Rh-positive" by lab #1 and "Rh-negative" by lab #2.
What would be your reporting protocol for these results? Would you have proceeded to a weak D test when faced with these results?
As a side issue I have received information second hand that a blood bank supervisor at a local hospital claims that: "Recent data shows that MANY donors typing as weak D possess a partial D phenotype and are at risk for RhD alloimmunization.". The problem that I have with this statement is the "MANY". Obviously partial D exists but I hsave never seen any information stating that it's anything other than a rare occurence.
Comments, as always, are appreciated.
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I validated anti-C3b,-C3d using buffered gel cards. We use 0.8% patient cells and we make the commercial Complement Check cells 0.8% too. We spin after a 5 minute incubation at room temperature. The check cells are always 3-4+. As for the sensitivity problems being discussed - negative tube vs + gel . . . why are you using gel? Up front we all know it is more sensitive. I don't think you can ignore a + gel result just because you repeat it in tubes and it is negative. My ped docs are enthralled with the increased DAT sensitivity. I have found 3 anti-Jka in gel that were negative with tube/PeG testing. Are they clinically significant? I can't ignore them.
I think when the situation arises in which you are deferring an unusually high number of apparently normal donors (as indicated in the OPUS104 post) one has to weigh the the value of a positive gel DAT when the tube test is negative against depleting your donor population. The question remains as to whether any of the DAT-negative patients/donors who were tested before gel existed suffered any pathological consequences because no one knew that their gel test would have been positive. In any case David your comment about the anti-C3 gel card is certainly useful information. Thanks!
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We are unfortunately beginning to defer donors on a regular basis due to positive DATs found at crossmatch with Gel cards at the hospitals we supply. The usual difference we find between tube and Gel is usually a factor of 2.(i.e. 1+tube=3+Gel) These donors (many of them VERY regular, long time donors) have no tube results at all.....but when the hospital Gel crossmatches the unit it is 1+ positive. This is very frustrating to both us and the donors. Many of them become upset over being defered and want us to explain IN DETAIL what the DAT means. You can imagine the long confusing conversations from here on....... the most important question is the one you posed, is it clinically significant?????????? We of course don't know so the donor gets defered.
This is exactly my concern. By reporting these gel results my guess would be that we are waving red flags that needn't be waved and as in your case deferring donors that needn't be deferred. Fortunately I am in a situation which does not involve crossmatching. In our case I would have a tendency to defer to tube DAT results. Tube was apparently good enough before the advent of gel; why wouldn't it be good enough now?
It would be interesting to see if Galvania's suggestion concerning washing the cells prior to use would clear up these gel crossmatch problems in your hospitals.
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Gel pos and tube neg - can happen as gel is more sensitive for Coombs than most tube methods. There is also a card (but as with the IgG/C3d card, I'm not sure if it's licensed in the States) that can differenciate between C3c (actually C3b) and C3d). Sometimes the pos gel test can be due to non-specific uptake of immune complexes. Usually washing a couple of times before putting on gel gets rid of these.
Thanks Galvania! I guess the next question would be: What is the clinical significance of a positive gel and a negative tube test?
I believe that most blood bankers here in the States perform tube DATs without the aid of a microscope. Would these gel+/tube- DATs be evident in the tube if they were examined microscopically? Has anyone looked at this? Thanks again for your response.
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When we started with Gel we did the IgG part in gel and the C3 in tube.
Our doctors (are suppose to) realize the sensitives issue of gel versus tube so thats not a problem but we test the eluate in gel as well and try to stay away from tubes.
We now use the combo IgG/C3 gel cards to do a DAT - if negative great.
If positive we then have to go back to the previous method of repeating the test with the IgG only gel and the C3 tube.
Thanks for the response. The correlation problem that I mentioned is that the poly gel card is positive and the tube test with poly, anti-IgG & anti-C3 is negative. Is anyone seeing this?
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Diamed makes a gel card that has an IgG, a C3d and a control well in each card (x2 TO make up the 6 wells). We get it through our Ortho supplier. It is wonderful, the rare time it is on back-order and we have to revert back to tube C3d testing the staff realize how lucky we are to have it!
Thanks for the info Janet but I'm not sure if this card is licensed in the States! I'll check with Ortho.
Missed Kells on Echo
in Equipment
Posted
Jeff,
Did you happen to test a different lot# of Capture Ready-Screen to see if it was perhaps a problem only with the lot you were using?
We've detected a couple of anti-Kells on the Echo, which is certainly not to say that we haven't missed any. But I have to totally agree with our friend from Nebraska who points out the fact that no testing system is perfect. To reach the highest level of sensitivity one should ideally run every specimen by both solid-phase and gel (and maybe throw a PEG tube screen in to boot).