Jump to content
Sign in to follow this  
Jennifer G

Anti-D unusual variability

Recommended Posts

Has anyone seen an Anti-D go from negative to 2+ positive to negative? We had negative antibody screens on an elderly A Negative woman from 2012 through 2018. 8 RBCs were transfused during this time. In August 2018, the antibody screen was 2+ positive, Anti-D was identified, and she received 1 RBC. In April 2019, the antibody screen was negative on 2 different occasions. The possibility of the August 2018 specimen being the wrong patient seems unlikely since we use hand-labeled separately armbanded specimens. However, I have never seen a true Anti-D behave this way.

Share this post


Link to post
Share on other sites

It might be a transient autoanti-LW, only reacting with D+ cells.

Genuine examples of anti-D are usually more persistent than the situation you outline, but never say never. An elderly person's immune system may work in unpredictable ways. On a related tangent....if it is a "real" anti-D, I would wonder about the source of immunization - I'm assuming D- RBCs were transfused. You do not mention platelet transfusions.

Share this post


Link to post
Share on other sites
13 hours ago, exlimey said:

It might be a transient autoanti-LW, only reacting with D+ cells.

Genuine examples of anti-D are usually more persistent than the situation you outline, but never say never. An elderly person's immune system may work in unpredictable ways. On a related tangent....if it is a "real" anti-D, I would wonder about the source of immunization - I'm assuming D- RBCs were transfused. You do not mention platelet transfusions.

Totally agree exlimey, however, another question I have is, ws a DAT performed when the "anti-D" was detected?  I also have another suggestion, to go along with your question about platelets, and that is it could be that one of the units was from a donor with a DEL phenotype.  Unless elutions (obviously) or molecular techniques are used, this may never be known, but it is known that some types of DEL can cause primary stimulation, but that the anti-D produced in these circumstances is very weak.  As you say exlimey, as the patient is elderly (and ill), the patient's immune system could be compromised.

Share this post


Link to post
Share on other sites
1 hour ago, Malcolm Needs said:

Totally agree exlimey, however, another question I have is, ws a DAT performed when the "anti-D" was detected?  I also have another suggestion, to go along with your question about platelets, and that is it could be that one of the units was from a donor with a DEL phenotype.  Unless elutions (obviously) or molecular techniques are used, this may never be known, but it is known that some types of DEL can cause primary stimulation, but that the anti-D produced in these circumstances is very weak.  As you say exlimey, as the patient is elderly (and ill), the patient's immune system could be compromised.

Excellent points. The diagnosis, i.e., the reason for transfusion, might also give a clue. I also thought about RH-IG, but I can't think of a traditional use for that product in an elderly patient.

Share this post


Link to post
Share on other sites
53 minutes ago, exlimey said:

I also thought about RH-IG, but I can't think of a traditional use for that product in an elderly patient.

Certainly in the UK, it is occasionally given to people of all ages who have idiopathic thrombocytopenia.

Share this post


Link to post
Share on other sites

Thanks for your replies! More info related to your comments... A DAT was not done at the time the antibody was identified, because the auto control in gel was negative. The patient has only received A Negative RBCs at our hospital (total of 9 at that time and 3 since then) and no platelets. She is a nursing home resident that was admitted for pneumonia, respiratory failure, and UTI. She has a previous history of coronary bypass surgery where she may have received blood products. Her platelet counts have always been in normal range 300-400s in our records. The DEL idea seems plausible to me. The Anti-D was relatively weak with reactions ranging from w+ to 2+.

Share this post


Link to post
Share on other sites

Another remote possibility: Passive anti-D from one of the transfused units ?

Most facilities are shy about transfusing red cells from donors with antibodies, but some of the savvy hospitals will get "favorable pricing" on Rh- units with anti-D. Since the Rh- unit (with anti-D) is typically going to an Rh- patient, the presence of the antibody is not usually a clinical problem, but may turn up as a laboratory anomaly. The amount of residual plasma in today's red cell products is very low, but a strong anti-D might show up post-transfusion and would probably only be seen be temporarily. You would have to look the timing of the transfusions and collection/detection of the anti-D-containing specimens. If you see a pattern, your blood supplier may be able to determine if any of the transfused units were from donors with anti-D.

Share this post


Link to post
Share on other sites

exlimey, again I agree, but it depends where Jennifer G is based.

NHSBT used to give out units of blood containing anti-D (and some other antibodies, as long as they were weak), but that is no longer so.  Since variant CJD raised its ugly head, we are no longer able to take blood from donors who have themselves been transfused (there are a few strange rules about when the blood was given, etc, but that is beside the point).  Because of this, and the fact that donors cannot be relied upon to be 100% honest (or simply don't know), so that we don't know if the antibody is as a result of a transfusion, a pregnancy or "naturally occurring", we destroy any units containing antibodies of any sort (with RARE exceptions), in case the antibody is the result of a transfusion, and it gets out into our untransfused inventory.

Share this post


Link to post
Share on other sites
Posted (edited)

Could the patient be on some sort of suppressant drug or steroid during the time when anti-D became negative? What is the diagnostics? 

Edited by Bb_in_the_rain

Share this post


Link to post
Share on other sites
1 hour ago, Malcolm Needs said:

exlimey, again I agree, but it depends where Jennifer G is based.

NHSBT used to give out units of blood containing anti-D (and some other antibodies, as long as they were weak), but that is no longer so.  Since variant CJD raised its ugly head, we are no longer able to take blood from donors who have themselves been transfused (there are a few strange rules about when the blood was given, etc, but that is beside the point).  Because of this, and the fact that donors cannot be relied upon to be 100% honest (or simply don't know), so that we don't know if the antibody is as a result of a transfusion, a pregnancy or "naturally occurring", we destroy any units containing antibodies of any sort (with RARE exceptions), in case the antibody is the result of a transfusion, and it gets out into our untransfused inventory.

Interesting. My perspective is from the USA. I assume then that the donors with detectable antibodies are permanently deferred ? That must put a hurt on the supply of Rh-.

Share this post


Link to post
Share on other sites
45 minutes ago, exlimey said:

Interesting. My perspective is from the USA. I assume then that the donors with detectable antibodies are permanently deferred ? That must put a hurt on the supply of Rh-.

Rh negative is more prevalent in Europe than US that European Blood Centers can afford to permanently defer donors with anti-D without hurting Rh neg supply? 

Share this post


Link to post
Share on other sites
22 minutes ago, Bb_in_the_rain said:

Rh negative is more prevalent in Europe than US that European Blood Centers can afford to permanently defer donors with anti-D without hurting Rh neg supply? 

This is very true.  There are certain areas of Europe (in particularly the Iberian Peninsula) where the percentage of D Negative individuals within the native population reach 25%.  This is all to do with enclaves where D Negative Palaeolithic people took refuge during the last Ice Age (about 24, 000 to 16, 000 years ago).  Other areas where this happened were the Balkans and Ukraine.

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now
Sign in to follow this  

  • Similar Content

    • By Jermin
      Hi All,
      I was wondering if antibody titre is performed on a pregnant mother who previously had HDFN. According to the books, it mentions 'After the first affected pregnancy, the antibody titer is no longer useful'. Therefore does it mean that it doesn't matter what the antibody titre level is, and should be referred to fetal medicine specialist regardless? Or if there is more to this, I would be grateful for some enlightenment 
    • By KtVl
      Hi all,
      I'm trying to find out the similarities and differences around the world (but particularly in Europe) for guidelines related to measuring fetomaternal haemorrhages and issue of anti-D.
      I'm particularly interested in which countries issue anti-D and don't estimate the FMH, what formulas countries use for calculating doses, what tests different countries use, whether the FMH is measured in whole blood or packed cells, whether different countries use the 1.22 muiltiplier to account for the different sizes of red cells... Not a small list I know.
      I've found a few international guidelines already so here are some useful links
      UK guidelines for all Transfusion related things are here http://www.b-s-h.org.uk/guidelines/
      Irish guideline on the use of Anti-D http://www.hse.ie/eng/about/Who/clinical/natclinprog/obsandgynaeprogramme/antidprevrhd.pdf
      Australian guideline on the use of anti-D https://www.ranzcog.edu.au/RANZCOG_SITE/media/DOCMAN-ARCHIVE/Guidelines for the use of Rh(D) Immunoglobulin (Anti-D) (C-Obs 6) Review November 2015.pdf
      Australia/New Zealand guideline on measurement of FMH https://www.anzsbt.org.au/data/documents/guidlines/ANZSBTguide_Nov02a.pdf
      Canadian guideline on the use of anti-D https://sogc.org/wp-content/uploads/2013/01/133E-CPG-September2003.pdf
      Please add links to this forum
      Many thanks,
      Katy Veale
       
    • By BloodbankZ
      What are other people's institutions practices on the following. If you have a patient with an anti-D do you need to go ahead and carry out the D antigen typing on the patients rbcs through the IAT phase(weak D testing)? The AABB 18TH ed. Technical Manual states on pg. 327 "When the D type of a patient is determined, a weak D test is not necessary except to assess the red cells of an infant whose mother is at risk of D immunization."  It then goes on to say under Identification of Antibodies to Red Cell Antigens pg.401 "Determining the phenotype of the autologous red cells is an important part of antibody identification."  We use MTS gel for as our primary method for blood type determination and it states that Most weak D antigen expressions will be detected(which means not all), however partial DVI epitope variant of the D antigen will not be detected with this monoclonal reagent. Not that it really changes how we transfuse the patient but just curious to others procedures/thoughts. Thanks in advance.
    • By rpp1
      How long does RHIG really persist?  The package insert says one thing, but with Rh-loving methods such as solid phase, I feel like I see RHIG hang around a lot longer. I think this has implication for pregnant mothers who have suffered from trauma or miscarriage prior to their current pregnancy.  Thoughts?
    • By txlabguy82
      Hi All,
       
      So I would like to present a scenario that happened to me and get your input.
       
      I received a specimen from the ED for ABO/Rh testing on a young female (she had a miscarriage, which at the time I was not aware).  We use the BD Pink (EDTA) blood bank tubes for all of our blood bank testing, this particular sample was about a little more than 1/4 of the way full (yes not the best sample, learned my lesson with this case) - there were no visible clots in the tube or in the cell suspension I made for testing (testing was done fairly quickly since it was only an ABO/Rh and we use a STATSpin centrifuge so I had results out within 20mins of it being collected). 
       
      These were my initial reactions at time of testing:
       
      Anti-A:         0
      Anti-B:         4+
      Anti-D:       w1+
      D Control:    0
      A1 Cells:      4+
      B Cells:        0
      Du:               3+
      Du Control:  0     CCC: 3+
       
      So of course my interpretation was B Positive, which was reported. (We use the monoclonal Anti-D)
       
      All of our samples are retested by another technologist if we have no previous history on the patient.  The samples sit at room temperature until they are tested and this was one was retested roughly 10 hours after my initial testing, these are the results:
       
      Anti-A:         0
      Anti-B:         4+
      Anti-D:          0
      D Control:    0
      A1 Cells:      4+
      B Cells:        0
      Du:               0    CCC:  3+
      Du Control:  0     CCC: 3+
       
      Interpretation:  B Negative
      It was tested 2 more times by two other techs later that morning and the report corrected and the patient had to be called back to get Rhogam injection. So of course and event report was initiated at that point for root cause analysis.  
       
      I was approached 3 days later after knowing nothing about what happened and told that I "miss-typed" a patient sample.  After reviewing the work card I of course said No I didn't because I actually remember working on this particular sample due to the fact that the D got stronger at AHG phase.  I was extremely puzzled by the results and pulled the sample at this point had been in the refrigerator for 3 days and found that the same had numerous large clots and lots of visible small clots in my cell suspension (however none of the previous techs noted or expressed this to my director).  
       
      I performed (3 days later) a forward and reverse typing (B Neg), DAT, and IAT.  The DAT (IgG and Poly) - Both negative (very sticky microscopically) and IAT in Gel was completely negative.  So at this point it was very perplexing as to what happened with the Anti-D.  Of course everyone my boss talked to said that this was impossible for the Anti-D to just disappear (I was not inferring that it disappeared to her) and I must have done something wrong, which really aggravates me to use the word "impossible" in medicine.  She said it was more logical that I mixed the control tube and the Anti-D tube at the AHG phase when I read the tubes which makes absolutely no sense to me (if the results were reversed from the results I got at immediate spin, then yes that would make sense and I would have questioned the results and started over).   
       
      OK, so here is my theory as to be the possible cause for this particular scenario has to do with a sub-optimal sample that was in the process of clotting at the time of initial testing - however I can only assume this theory and I know that it didn't interfere with the Anti-A or Control on the forward type, but these are all different antiseras with different blends of antibodies/proteins, etc.. I am thinking that since I didn't see or detect clots when I tested the EDTA sample the first time it is possible that something during the clotting process potentially interfered with the Anti-D causing it to be a false positive. Since the specimen wasn't tested again until 10 hours later when the clotting process was definitely complete there is no way to prove this, unless someone where to have retested it immediately after I performed the first test.  We've seen cold autoantibodies disappear after sitting at room temperature due to autoadsorption, who is to say that since the clotting process was complete whatever was causing the interference may have been gone 10 hours later when the full clots formed.   My boss refuses to even think this is remotely a possible and I had to have made an error, she said we use to use plain red clotted tubes all the time for blood bank and never had any problems (don't think she is getting that these tubes have no additive and normally the clotting process was a lot faster in plain red tubes with no additive. Then again she also couldn't understand how a clot would get stronger overtime (I wanted to bang my head on the desk with that remark).  If I made an error or potentially made an error I would definitely own up to it, but in this instance her suggestion that I switched the test tubes around and reading the control as the patient makes no sense what so ever. 
       
      Has anyone every encountered anything like this before and what is your thoughts on the potential reason for the various reactions between a 10 hour period?
       
      Thanks,
      -TxLabGuy82
  • Advertisement

×
×
  • Create New...

Important Information

We have placed cookies on your device to help make this website better. You can adjust your cookie settings, otherwise we'll assume you're okay to continue.