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Found 10 results

  1. Hi All, We are about to move from using Bio-Rad IH-1000 to Immunocor NEO in our blood bank department. As most of you are already aware, the IH-1000 uses column agglutination technology (CAT), whereas the NEO uses Solid Phase Red Cell Adherence (SPRCA) assay. SPRCA is known to be more sensitive, which is great when picking up on elusive antibodies belonging to Kidd blood group system (I think ). My concern is about the techniques which employ the use of indicator cells that are coated with anti-IgG. It will only pick up on IgG antibodies and none of the IgM antibodies. How significant is this? Is there any way of picking up IgM antibodies using such technique? Or should we not worry since IgM antibody does not usually reaction at 37C? Regards, Jermin
  2. Hi All, I have a question, but firstly good old story time for some context. I came across a patient who had positive antibody screen on all three screening cells used (BioRad). I was concerned this may be an auto and pan-reactive, and required units. Performed a monospecific DAT, showing a positive reaction to IgG only. By this time antibody panel finished cooking and showed the patient may have anti-Fya , but couldn't do phenotype. By this time I was nearing my shift so handed it over to my colleague and asked for some units to be crossmatched. However, he refused as DAT was positive and said he rather send the sample to reference laboratory for them to crossmatch. The next day I crossmatched units to verify if it could have been done in our laboratory (just because I am sad that way), and turn out the unit I crossmatched was compatible (which I wasn't surprised about) Question Why does positive DAT (or the cause of positive DAT) sometimes interfere with IAT techniques (such as antibody panel and crossmatch) and sometimes it does not? If both use AHG, then wouldn't positive DAT with IgG cause antibody panels shows pan-reactive with red cells? But obviously it doesn't, but I'm trying to figure out why, and I'm sure the answer is quite obvious. My laboratory seems very hesitant whenever they see anything regarding autoantibodies or positive DAT, and thinks that sample cannot be crossmatched in-house and needs to be sent off without even trying to investigate. Hopefully, by me asking this question, I can explain it back to my colleagues (but obviously take all the credit). Cheers in advance, Jermin
  3. 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
  4. Is there a good explanation in a technical manual to better explain to my co workers how to handle this situation : positive antibody screen with a negative antibody panel
  5. Okay so I was always taught to use the rule of 3, 3 positive reactions and 3 negative reactions for peforming an antibody ID. I was also taught to always use homozygous positive and negative cells whenever possible. Sometimes of course it is not due to low incident/high incident antigens. I do know you need to use a homozygous cell when performing "rule outs". What is everyone else's practices and thoughts as I need to clarify our current antibody identification policy. Thanks in advance.
  6. Dear My Colleagues, I am confused about which sample should be used in detection cold antibody, either allo or auto? Shall I use serum or plasma? Or both are suitable… My confusion arise from statement that, IgM depend on complement in its action and plasma has no complement….!!!!! Thanks.
  7. A patient came to the ICU with Hb at 52. It was quickly concluded that he had some sort of hemolytic anemia. He also had an immunodeficiency since birth with low levels of both IgG and IgA, and was wholly uncapable of producing IgM. The doctor requested a monospecific DAT and a screen, and ordered 2 bags of blood. All my lab tests came out as 3+ straight over, including the ctl well, so I proceeded with an antibody identification. Unsurprisingly, the patient's plasma gave 3+ reactions against all panel cells as well as his own rbc's, both with IAT/LISS (gel) and PEG. Autoadsorption x2 gave no other outcome, not even the slightest reduction of reactions. I cross-matched blood (again, 3+ reactions) which the patient received without any reported transfusion reactions. When I had the results from the cold ab panel on NaCl gel cards it clearly showed an anti-e at all temperatures (4, 20 and 37°C). Since the panel is used to identify IgM antibodies I assume that this is an autoantibody of IgM-type, and not a regular IgG anti-e, possibly caused by the IVIg the patient has received? I have no clue. The hospital where I work isn't very large and we don't do any advanced ab identifications ourselves, neither do we encounter these kinds of results and patients regularly. Is there anybody who has some ideas and would like to enlighten me? Would you have done any further investigation regarding ab detection?
  8. Can anyone tell me if we have a universal way in identifying an antibody using panels? Are there any textbooks available for students that cover these steps?
  9. Does anyone have any procedures that they can share for making up student specimens, either spiking plasma samples with antibodies but even more so, making up specimens for doing eluates? If there are some on this site already, sorry for the repeat, but I can't find them.
  10. Our current policy for transfusing our sickle patients is to honor their Rh and Kell phenotypes until they form a clinically significant antibody. At that point we will honor their full phenotype as they are considered a responder. But if they form a clinically insignificant antibody, we continue to honor only the Rh and Kell phenotype. Are only patients who form clinically significant antibodies considered responders? This has become a topic of conversation at our hospital and no one is sure what the correct answer is. If any one has any info that would shed some light is would be greatly appreciated!! Thanks!! (Also, if you have any articles siting this it would be even better!!)
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