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  1. Patient with bowel issues presented with serious haemoloysis, Hb dropped to below 60g/L. Frank haemolysis apparent but DAT was completely negative, Ab screen/IAT and enzyme IAT panel neg, auto negative, eluate neg vs panel by IAT. Consultant Haematologist suggested performing T activation studies. Patient was found to be Tk activated, but Tk activation not associated with haemolysis. I have heard on the grape vine that Tk activation is associated with acquired B phenotype. Patient was group A with anti-B. Current ABO typing reagents do not detect acquired B, so we do not know whether this patient had acquired B. Hypothetically, could haemolysis occur with acquired B? Could the patient's naturally occurring anti-B haemolyse the 'acquired B' red cells???
  2. In my lab we have investigated a number of patients who are on CD47 therapy. They are always strongly pan-reactive by gel IAT, enzyme IAT and LISS tube IAT, but auto negative and DAT negative. If they do have antibody bound to their red cells, why are they DAT negative? Is it a similar mechanism as anti-CD38 therapy? Where DARA induces loss on CD38 on red cell surface, and so protects red cells from haemolysis?
  3. Hello, In my reference laboratory, we have a renal transplant patient with multiple antibodies; anti-D, anti-K and anti-Fya. The patient had always been DAT positive and we had been unable to type for Fya. Finally got around to genotyping, and were surprised to find that the patient is Fya positive. A quick read up suggested that Fya can be involved in renal allograft rejection. If the patient received a Fy(a-) kidney, could the auto-Fya have originated from that? Not ever seen an auto-Fya before, and wondered if it was more common in renal transplant, or purely coincidental? Kind regards Alison
  4. Thanks for the quick reply. Good to know that I am not the only one who had not heard of this.
  5. Hello all, I work in a reference laboratory in the UK. We referred a sample for further investigation to another reference laboratory. The report that we had back found the following Anti-P1 microscopically by 18C direct agglutination with cells that have strong P1 expression. No reactivity in LISS IAT with untreated or papainised cells. The patient's cells were found to react extremely weakly with two examples of anti-P1, compared to much stronger reactions with known P1+weak control cells. This finding is likely due to suppression of the patient's P1 antigen, which is not uncommon in pregnancy. I was not aware of suppression of P1 in pregnancy and could not find any references in Blood Group Antigen Facts Book or Geoff Daniels Human Blood Groups. Could anyone shed any light on the mechanism and some helpful references? Kind regards Alison
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