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I agree 100% with you that anti-Vel can be a real problem, but that problem can be a real problem not just when the antibody is new. It is one of the few antibodies that are best detected by the two-stage indirect antiglobulin technique (see Geoff Daniels' book, Human Blood Groups), but I don't know of anyone in the world who uses that technique as a routine. The reason that this is the best technique to use for anti-Vel is that it is much more easily detected with anti-C3d than either anti-IgM or anti-IgG, however, of course, in these days of automation, most people use samples that have been anti-coagulated with EDTA. This means that the calcium, magnesium and manganese ions required as co-factors in the initiation of the classical complement pathway are not available, and so we no longer see the tell-tale haemolysis in our tests that is normally seen with an anti-Vel (and, of course with ABO antibodies, some anti-I antibodies from an adult i individual, anti-P+Pk+P1 from a p individual, and IgG anti-Lea). Indeed, I think I have noted on Pathlabtalk before that I know of one case of anti-Vel that proved to be fatal, which was only ever detected in a clotted sample from the patient, but NEVER in an EDTA sample.

Vel, as always, I appreciate your response, Malcolm. Scott

I just answered this question. My Score PASS

I just answered this question. My Score PASS

I just answered this question. My Score PASS

Sorry Scott. In my personal opinion, and it is only my personal opinion, it's not 20th century........it is at best 18th century!!!!!!!!

Absolutely the advice given to you was correct. For a start off, as you say yourself, 80% of A2B individuals do NOT make an anti-A1, but of those 20% who DO make an anti-A1, how many will make that anti-A1 as a result of immunisation as a result of transfusion or pregnancy? The answer to that, if you read any book concerning blood group serology (and that is NOT a criticism of you - we all started somewhere, including the very best, such as Herr Dr Willy Flegel, and others - and I have HUGE respect for Willy), you will see that a clinically significant anti-A1 is amazingly rare. For an anti-A1 to be clinically significant, it has to react strictly at 37oC, and that is a VERY rare "animal", and no example of anti-A1 has EVER been implicated in a case of HDFN, so, PLEASE, do not worry about giving A1B (or even A1) blood to an A2B individual, even if they have an anti-A1 in their circulation, UNLESS they have an anti-A1 that is actually active at strictly 37oC.

BYOB, I suggest.

Even docs don't understand BB. We had a pediatric registrar who was insisting on issue of O Rh negative FFP to a 3 yr old baby with B Positive blood group who had suddenly started bleeding at night and we didn't have any B group FFP in stock. He was refusing to accept AB group FFP which the tech had thawed. I had to step in & talk to consultant at 2 am & convince him for them to accept AB Group FFP.