johna
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Everything posted by johna
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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).
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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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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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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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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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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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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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----------------------------------------------------- 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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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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"Rh-positive" vs. "Rh-positive, weak D" protocol
johna replied to johna's topic in Immunohematology Reference Laboratories
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. -
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 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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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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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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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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Thanks for the info Janet but I'm not sure if this card is licensed in the States! I'll check with Ortho.
