Malcolm Needs

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I would thoroughly recommend that you contact Rachel Moss Hibbttt at Imperial College Healthcare NHS Trust.

Thanks gagpinks. Fine, but is the patient of anything other than (I'm not sure how to put this without offending people, but here goes) of pure UK ethnicity? As the patient is of child-bearing potential, AND is transfusion-dependent, I am CONVINCED that RCI should have taken the investigation further!

Interesting case, and I agree entirely that the patient should be excluded from electronic issue, but how this decision be made known to any other hospital? I am somewhat surprised that the RCI Laboratory did not pursue the case further, unless no further samples were available, given that the patient underwent a classic acute haemolytic transfusion reaction, but I would also dispute that they tested the plasma against many (sufficient) low prevalence antigens. Of those you list, Do(a), Do(b), Lu(a) and Kp(a) would all be classified as polymorphic in the UK greater than1% expression in the population - although I fully realise that this classification is NOT the same throughout the world), and Co(a) is a HIGH prevalence antigen. In reality, therefore, the only low prevalence antigen against which they appear to have tested the plasma is Wr(a). It may be helpful in such a case to know the ethnicity of the patient, the sex and, if female, any pregnancies (and if these all went to term, or were any of the babies affected by HDFN), and, if the male partner is still available, whether or not his red cells could be typed and, possibly, tested against the patient's plasma (assuming for the moment, the patient is a female). I really am somewhat amazed that the RCI Laboratory did not submit a sample to the IBGRL.

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No. Anti-Ce (anti-Rh7) is an antibody directed against the "compound antigen" Ce. In other words, the RHC and RHe genes have to be from the same haplotype. I suppose you could look at the antibody as being analogous to anti-ce (anti-f), which would react with, for example, red cells from an individual who has the Rh genotype of DCE/dce (I KNOW there is no RHd gene!), or Rzr, but not with, for example, red cells from an individual who has the Rh genotype of DCe/DcE, even though both the c and the e antigens are expressed on the red cells. What I was saying is that anti-Ce, per se, will only react with red cells where both the C and e antigens are derived from the same Rh haplotype (such as DCe), but, unless there is an element of monospecific anti-C present, the anti-Ce will not react with, for example, red cells that are from an individual with the Rh genotype of DCE/dce, as the C antigen and the e antigen are derived from two different haplotypes. Of course, if there is an element of anti-e as well, THEN the reagent will also react with the e antigen, but anti-Ce is much more frequently a contaminant of an anti-C than is an anti-e. I'm still not certain I have explained that as clearly as could others, but I am trying my best!!!!!!

I'm afraid I still can't agree with this methodology, for a couple of reasons. Firstly, antibody/antigen reactions are, largely, governed by the Law of Mass Action. As a result, and given a steady state of conditions (e.g. temperature), however long the incubation time may be, once a state of equilibrium is reached, there will be no net gain of antibody coating antigens, however long the incubation time may be extended. Certainly, LISS will increase the rate of association of antibody and antigen enormously, but this will apply equally to the auto-antibody as any allo-antibody that may be present, however, of course, some antibodies will only react visibly with red cells that have homozygous expression of a particular antigen, and, if such an antibody is present, it will be very difficult to detect in the presence of an auto-antibody, but can still cause a haemolytic transfusion reaction, albeit, usually a delayed reaction, but it can still cause damage to the renal system in particular. For these reason, I would always perform an adsorption, to get rid of the auto-antibody, even if I had no intention of performing specificity tests on the auto-antibody (although, it goes without saying, I would go all out to try to ascertain the specificity of any allo-antibody detected). I am trying to write a book at the moment, called "Human Red Cell Serology and Blood Groups for Beginners", and Chapter 2 deals with Serological Techniques. I attach the draft copy, which also gives relevant references, the odd diagram and abbreviations I use throughout the various chapters. Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories.docx Chapter 2 Serological Techniques in Routine Blood Transfusion and Red Cell Immunohaematology Laboratories Figures.docx Abbreviations.docx

In what way does a LISS screen with 30' incubation "CONFIRM" that there are no underlying clinically significant allo-antibodies present? I am always happy to learn.