Lisa J

Many thanks for the replies all!

Oh my goodness that sounds truly terrifying!

In the words of Homer Simpson Doh!!!!! That teaches me not to read my guidelines thoroughly!!! Thanks for the answer Malcolm....supplied with great detail as I expected!! Well the little one is now 8 this year and I have produced another more naughtier version who is now 5!! How time flies I remember seeing your little lad in pics years ago and now he is helping you with presentations...a chip of the old block eh? How time flies!! I am still at the same place but have moved into the TO post so not based predominatly in BT but its still what floats my boat!! Would there be any chance I could come and have a look at how you deal with these samples it would be a great chance to pass on the knowldege to our Bt trainees who are terrified when something unusual crosses our paths! Many thanks again Malcolm this forum is really helpfull:D

Hi I would be gratefull to hear any feedback on how other labs approach this issue, many thanks for reading! We recently had a patient with a pan reactive autoantibody that needed 4 units cross matched for routine surgey. The 3 cell antibody screen and IAT and papain panel cells were all positive (the patient had not been transfused with any blood products since since 2009) and the DAT was positive for IgG and C3d. We referred the sample to our local reference centre who performed an autoadsorbtion and found no clinically significant alloantibodies and recomended that we provide ABO/D and K compatible units for cross match. My query is regarding the subsequent tests that need to be performed before the issue of red cells by our laboratory. We are a small lab and dont come across these patients very often and are wondering how other laboratories deal with these issues as we have a slight difference of opinion!! As we have no autoantibody depleted serum to work with (as this is at the reference centre) but we do have an aditional EDTA sample on the patient should we select the ABO/D and K compatible units as advised and: Perform an immediate spin crossmatch and issue the units? or Perform a cross match with all 4 units using the recipient serum and also set up an auto and only issue the units if they are equal to or weaker in reaction strenght to the cross match? I understand the logic for the first one but not for the latter completely........We have been told there are no atypical red cell antibodies in the patients serum so what is the purpose of comparing the auto to the crossmatch reactions? The patient has a pan reactive non clinically significant antibody that is reacting with an antigen expressed on the screening cells/panel cells and donor red cells.....even if the reaction is stronger with the donor cells could this be due to the donor cells expressing more of that antigen than the patient? Say one of the 4 units crossmatched comes up as a strong positive when compared to the other three units that are equal to the auto reaction...........could that indicate that the patient may have an antibody to a low frequency antigen expressed on the donor cells that is not on the panel/screening cells, or would that be masked by the auto antibody anyway or would it contribute to a stronger reaction? Should that sample then have further antibody investigation work done on it? Very interested in hearing others opinions many thanks lisa J (UK)

Hello all, hope some of you may be able to help me out or just point me in the write direction, I am running some tutorials sessions at work and we have just covered the subject of A subgroups. We have some conflicting information regarding this subject and I wondered if anyone can explain this. Are A subgroups such as A2 etc caused by a mutation of the A gene which results in less A antigen being transfered to H subtsance on the red cells (Due to a less effective transferase enzyme) than A1 cells or in addition to the less effective enzyme is there also a structural difference between the A1 antigen and A2/A3 (etc) antigens etc? I would be very interested in any links to relevant atricles in this aea. many thanks Lisa

Thanks Malcolm I thought that would be the case just wondered if anyone in the UK had already done that!

Does anyone who uses the Medialab system for training in the UK know how the CE credits on the on-line courses relate to IBMS CPD credits? We are trying to encourage staff to take more of the on-line courses and it would be nice to allocate IBMS CPD points for the courses by way of encouragement

Many thanks Malcolm, just needed to hear what I already thought....and yes I am Lisa from the tooting area! But no longer in Tooting....now in Kent! But still working in London !

Hi there, I would be really interested to hear other blood bankers opinions on the following scenario: We have a patient with an autoantibody who is transfused 2 units red cells approx once every 2-3 weeks. I have always understood that patients with autoantibodies should have the autoantibodies adbsorbed from the sample (either in house or by a reference lab) in order to detect any underlying red cell antibodies that may be produced, and that this should be perfromed on every occasion that the patient requires blood to ensure that the lab is detecteding any recently produced red celll antibodies from recent transfusions. Some colleagues of mine have stated that this does not need to be done and that you can cross match red cell units against the patients plasma and as long as they are less reactive than an auto then it is OK to issue units to the patient. They do not do panels on this patient as the autoantibody results in psoitive reactions in all panel cells so 'it is of little use'. What do other labs do in this scenario? I am not happy to issue units in this way and would prefer an adsorbtion to be done first and then run a panel to determine the presence of any other underlying masked red cell antibodies and then do a cross match. If the patient has a very weak underlying red cell antibody that is masked by an autoantibody and the unit that is selected for xm has a heterozygous expression of the corresponding antigen, surely this weak reaction in the xm could be masked by the presence of the autoantibody and the reaction may well be as weak as the auto leading to the issdue of the unit and a possable delyed transfusion reaction? Would be very interested to hear others opinions I