Malcolm Needs

Unfortunately, although that is the paper, I can't seem to access it on-line either, and I haven't got a copy I could scan for you. On top of that, both Steve and Alan are retired, and I haven't got contact details for either of them. Sorry. You could try using the attached form? immunohematology_reprint_application_2019.pdf

Welcome mTOR. Is your first name "caveat"? Sorry - my bad!

The first thing to say is that the laboratory personnel cannot diagnose a transfusion reaction. This may be a delayed haemolytic transfusion reaction, where the patient is clinically compromised, or it may be a delayed serological transfusion reaction, where the sample from the patient tests for a positive DAT and a "new" antibody specificity, that can be eluted from the red cells, but where the patient is not clinically compromised. This can only be diagnosed by the physician looking after the patient. Secondly, the anti-Jka may be a de novo specificity, or may be present in the circulation as a result of an anamnestic reaction. Certainly, two weeks seems a bit quick for a de novo specificity to be detected, but it can happen (never say never in blood transfusion!), so it is more likely to be present as a result of an anamnestic reaction, although there must be a certain proportion of IgM immunoglobulin, as well as IgG. As yan xia says, Kidd antibodies can cause complement fixation, but can only so do if there is some element of IgM present (anti-Jka that is pure IgG cannot fix complement), however, it is incredibly rare for Rh antibodies to fix complement (as far as I know, there are only two examples of anti-D described in the literature that have been able to fix complement - and just think how many millions of anti-D have been detected), so the complement on your patient's red cells is much more likely to be there as a result of the anti-Jka, than the anti-E. Adding fresh serum does increase the sensitivity of the test (the so-called "two-stage IAT"), but treating the red cells with a protolytic enzyme, such as papain, and then performing the IAT is even more sensitive. An eluate can be used to "concentrate" the antibody sensitising the patient's red cells, but, be careful, as, is you are using a commercial elution kit, this may go counter to the kit instructions.

Welcome LaShandra Harris.

Almost certainly not. Although Race and Sanger wrote about this phenomenon (very briefly) in their book, "Blood Groups in Man", I remember very distinctly Ruth Sanger telling me that she have grave doubts that such a phenomenon actually existed.

I think you would probably find this in our UK Guidelines, if you put "BCSH Guidelines" or "BSH Guidelines" (they have recently changed their name) into your search engine, you should find Guidelines about anti-D immunoglobulin, and you should find it in there. If not, get back to me and I will have a look in my text books.

Oh yes, we would give anti-D immunoglobulin in such a case, but, if it were a case of identity theft, and the recipient made allo-anti-D, and it went to court, the thief would not win!

Welcome SLACOUR.

Welcome Vivek.

Oh true Scott. All I'm saying is that, even if the platelets are a different (incompatible) ABO and Rh type, it wouldn't be too much of a problem, except in a baby or very small child.

The Rh antibody specificities involved in WAIHA are usually something like anti-Rh17 or anti-Rh18, which are antibodies that are directed against antigens that are almost expressed universally on all human red cells, except those of very rare individuals with deletion or partial deletion of Rh antigens. That having been said, these antibodies very often mimic other specificities, such as, for example, an auto-anti-e, but can be adsorbed to extinction by red cells apparently not expressing the antigen. In other words, the apparent auto-anti-e can be completely adsorbed by using DcE/DcE (R2R2) red cells that are, of course, e Negative. This is because the DcE/DcE (R2R2) red cells will express both the Rh17 and Rh18 antigens, which are the antigens that the auto-antibody specificity is actually directed. There are other specificities that can be involved in WAIHA outside of the Rh Blood Group System (such as auto-anti-Wrb), but these are much rarer. As far as your second point is concerned, I attach three PowerPoint slides. The first is a diagram of how we go about looking at antibodies, the second is a photograph showing the store of some 400 rare red cells frozen down for use in RCI investigations, and the third is a (very untidy looking - but we know where everything is located) freezer full of very rare antisera, so that we can "attack" a problem from both sides, if necessary, by looking at the antibody in the patient's plasma, and/or the (usually) high prevalence antigen lacking from the patient's red cells. Armed with information, such as the ethnicity of the patient (not politically correct these days, but HUGELY important), and how the antibody reacts with red cells treated with various enzymes and chemicals, we can narrow down the specificity without having to use, and possibly waste, a large number of different rare red cells and antibodies. Antibody algorithm..ppt

Hi tsanders0703, yes, this phenomenon is actually not that unusual. The anti-D immunoglobulin in the maternal circulation will have a lower concentration than that in the foetal circulation because the IgG immunoglobulins are actively transported across the placenta. However, because the maternal red cells do not express the D antigen, it will appear that the concentration of the anti-D immunoglobulin in the maternal circulation is higher than that in the foetal circulation, as that transported to the foetal circulation will be adsorbed onto the D antigen expressed on the foetal red cells; hence, there is detectable anti-D in the maternal plasma, but not necessarily in the foetal plasma, but the foetal red cells are DAT Positive. As long as the mother has been shown not to have any atypical alloantibodies in her plasma during the pregnancy, then there really is no need to perform a DAT on the cord sample. In the UK, this is actively discouraged by our Guidelines, if the mother is definitely known to have been given prophylactic anti-D immunoglobulin during her pregnancy. Although the baby's red cells may well be DAT Positive, there really is no need to perform an elution, as the amount of anti-D adsorbed onto their red cells will be insufficient (by a considerable amount) to cause any clinically significant haemolysis (and, remember, there is always quite a drop in haemoglobin concentration anyway soon after birth). If, however, the baby shows any CLINICAL SYMPTOMS of HDFN, then all tests should be performed, as the mother may have made an antibody against a low prevalence antigen that is expressed on both the paternal and baby's red cells that is not necessarily expressed on any of your screening or panel cells.

Welcome simplyshadey.

Welcome BB Brooke.

Welcome bbksa101.

Not in the UK gagpinks. The chances of someone else needing platelets of an identical name, hospital number and date of birth are remote, as to be disappearingly likely, and, in any case, the amount of plasma involved is not likely to cause a transfusion reaction in an adult. Lastly, if they needed HLA-matched platelets, at worst, the platelets would not last too long in the circulation, but would not cause a reaction.

I know you are in the USA, but you might find the BSH Guidelines on the subject useful. Just put "BSH Guidelines" into your search engine, and go from there!

Welcome BldBnkLvr.

Welcome JJSPLAYHOUSE.

Welcome Jimbo.

Welcome Tdawg.

It almost certainly would, but, of course, the dose would be considerably higher.

Welcome pathlabtech.

Welcome A Dunbar.

Welcome mmeagley.