Malcolm Needs

I THINK there are figures in the earlier "Mollison's (but I am relying on a notoriously bad memory). Personally, only a few (in 43 years), but there are figures annually in the UK SHOT Reports (Severe Hazards of Transfusion).

Why do they want to know the titre of IgG anti-A or anti-B? It has been known for decades that the titre makes no prediction of the severity of ABO HDFN? The only real predictor is that the foetus/newborn will suffer at the same gestational period, or earlier, than the previous pregnancy, and to the same extent, or worse, than in the previous pregnancy. The problem comes with the first pregnancy, but, as titre is not predictive, surely it would be sufficient for the doctors to know whether or not IgG ABO antibodies are present in the maternal circulation in the first place? I realise the IgG ABO titre is very relevant in solid organ transplants and stem cell transplants, or have I missed something?

I would be wary of relying on enzyme-treated red cells, as a negative reaction could be due to the cognate antigen being denatured by the particular enzyme used.

The trouble is that, if the antibody happened to be an anti-Jka or, worse, an anti-Vel, the resulting rise in titre, following an anamnestic response, could be fatal on rare occasions.

Welcome jack323.

Extended cross-match, UNLESS, the history of which other hospitals the patient has been treated is known. Of course, in the UK we have a national database of patient's antibodies, which makes life an awful lot easier, even if the data is just a "snap shop".

The trouble was that, in those days the anti-D immunoglobulin was known as "anti-D for Mum's Bums" in the UK, as the shot was given in the gluteal muscle. But, there was an awful lot of fat in that muscle, so the anti-D had a habit of "staying there", rather than being adsorbed into the blood stream. This meant that, even when the dose of anti-D immunoglobulin was calculated from the Kleihauer-Bekte test, the actual dose reaching the circulation was far lower than the calculated dose, and women used to produce allo-anti-D as a result. Nowadays (at least in the UK) the shot is given in the lateral deltoid muscle, where there is a good deal less fat, and so the shot is adsorbed into the circulation much easier, and so there are fewer cases of maternal allo-anti-D. I realise that this is a very vague explanation, and that there are many other causes of anti-D immunoglobulin being less than effective (such as giving it to the father, or even to the ambulance staff (SHOULD be unbelievable, but is actually true), but it does show just how complicated such a simple thing as this can be.

Welcome MS2005.

Welcome MelanieQ.

Welcome JT Super.

Welcome MELANIE E. G..

Welcome Cautious Carol.

Welcome K Kindy.

Have you thought of thumb screws????????!!!!!!!!!!!!!!!!!!!!

Agreed. The ONLY time we might perform anything like a post-partum screen is if the baby's DAT is positive, and the baby has clinical signs of HDFN, but the mother has not been shown to have an alloantibody in her circulation during the pregnancy. In such a case, we may well test the maternal plasma (or an ABO adsorbed and eluted sample of the plasma) against the paternal red cells (if available) to see if the antibody is directed against a low prevalence antigen expressed on the paternal red cells. Having said that, however, this would only be useful in a further pregnancy with the same male, as providing the present baby with a unit for top-up or exchange would be easy if the antibody is directed against a low prevalence antigen

Absolutely correct Marilyn. In those days (1963, I was in infant/junior school and 1967, I had JUST started secondary school) I THINK we were only using whole blood for red cell transfusions, but I wouldn't know for certain.

By 1967, there at least two examples of an allo-antibody in a unit of blood causing a transfusion reaction with a unit transfused that expressed the cognate antigen, so this phenomenon is not unknown, as Neil Blumberg intimated above (Zettner A, Bove JR. Hemolytic transfusion reaction due to inter-donor in compatibility. Transfusion 1963; 3: 48-51, and Franciosi RA, Awer E, Santana M. Interdonor incompatibility resulting in anuria. Transfusion, Philad 1967; 7: 297-298, both cited in Race RR and Sanger R. Blood Groups in Man, 6th edition, 1975, p.302, Blackwell Scientific Publications, Oxford). Unfortunately, I am no position to answer your other questions.

Welcome Melanie Oliveira.

In the UK, such a unit would be offered to the National Frozen Blood Bank, and would only be frozen AFTER a thorough aseptic wash, followed by addition of a chemical to prevent the formation of sharp ice crystals, and then more washing upon thawing. There would be no allo-anti-Kpb left!

We used to, when I first started working in a hospital, but, since the advent of vCJD, after which we could never be certain whether an allo-antibody had been caused by a transfusion or pregnancy (well, in a female anyway!!!!!!!!!), and so we no longer use a unit for transfusion if an allo-antibody is present in the circulation of the donor.

Welcome sanaa.

Welcome psykobillys.

This PowerPoint Lecture gives some idea about how we approach things in the UK. It may well be different in other countries. In Depth Lecture on Alloimmune Haemolytic Disease of the Foetus and Newborn HDFN.pptx

The UK has (I was one of the co-authors). Guideline for blood grouping and red cell antibody testing in pregnancy. White, J, Qureshi, H, Massey, E, Needs, M, Byrne, G, Daniels, G, Allard S, British Committee for Standards in Haematology. Transfusion Medicine, 2016, 26, 246–263. doi: 10.1111/tme.12299.

Well, the first thing to say is that red cells CANNOT be either homozygous or heterozygous (or, come to that, hemizygous). These terms apply ONLY to genes, and red cells do not contain a nucleus. The antigens can only be described as, at best, "homozygous", "heterozygous" or "hemizygous" expression, or, alternatively, "double" or "single dose" expression. Then, it HAS to be accepted that, unless the maternal antibody is an autoantibody, it must be an alloantibody (or, possibly, an isoantibody), which means that to mimic the state of the foetal red cells, the red cells used to titrate the antibody MUST have a "single dose" expression. However, that in itself presupposes that the foetal red cell antigens are all expressed at the same time, which we know is untrue (just look at the A, B and H antigens as an obvious example, but also the Kell antigens that are expressed much earlier than are the Rh antigens) or are ONLY expressed on foetal red cells, as opposed to other tissues (such as on the placental cells, which have, in some cases, been proved to adsorb the maternal antibodies). Then, there is the fact that not all antibodies can be detected by all techniques. This is why Reference Laboratories SHOULD have more than one technology available (and their workers should be provably competent in these techniques. However, even then, not all techniques can predict the severity or otherwise of HDFN. For example, antibodies within the Indian Blood Group System always show that they can cause severe HDFN by certain techniques, such as MMA, but they don't! There is also the fact that the immunoglobulins may be IgM, IgA, IgG1, IgG2, IgG3 and IgG4 (to mention just a few), and I have yet to come across, or read about, an IgG4 immunoglobulin causing HDFN. So, my answer is that there is a HUGE amount of knowledge known about the various antibody specificities, their titres, the expression of their cognate antigen, etc, etc, that there CANNOT be a single answer to your excellent question, but that the best thing that can be done is to read around the subject - and read around the subject from every source available - not just from a single country. OKAY THEN, RIP ME APART!!!!!!!!!!!