Malcolm Needs

The antibodies used for routine ABO and D typing these days are almost universally blended monoclonal antibodies. They are incredibly strong, but they are also highly specific. An individual with a particularly weak expression of either the A or the B antigen may not express all of the epitopes on all of the various "backbone" carbohydrate molecules that express the A or B antigen, Because the monoclonal antibodies are so specific, they may not contain the "correct" specificities to sensitise some of the weaker antigens. Anti-A and anti-B derived from a human will be polyclonal, and, because of this, these antibodies may not be as strong as the monoclonal antibodies, but they will also be less specific (they are likely to be a whole "soup" of either anti-A or anti-B specificities), and are, therefore, much more likely to sensitise most, or all of the various epitopes. Because of this, if only a few epitopes are expressed, they are much more likely to be sensitised by polyclonal antibodies than monoclonal antibodies. Obtaining human-derived anti-A and anti-B from a commercial company these days has become very difficult, to say the least. Many people are using either patient-derived plasma, or donor-derived plasma, but, if you are going to use these sources, it would probably be a good idea to perform a quick titration to ensure that they are of a reasonable strength (128 as a minimum), but they should be thoroughly tested to ensure that there no other specificities "hiding" under the desired ABO specificities. As for the method, the optimum temperature for IgM is about 4oC, and so the tests should be incubated in the cold, and quite possibly the red cells should be treated with a proteolytic enzyme, such as papain or ficin. As for the elution method, the Lui method is very good for ABO elutions, but, equally, the old-fashioned method of elution at 56oC also works well, but needs to be constantly shaken until the eluate is separated from the red cells. I hope that is of some value to you.

Welcome khovis.

They certainly do in many hospitals within the UK where Biomedical Scientists have been empowered to so do. I should point out that blood is never withheld in an emergency situation, there will most certainly be an investigation after the event.

Certainly in the UK, if they are known to be sickle cell positive, whether trait or disease, are supposed to have HbS Negative blood. I should also have added that a huge percentage of our units are tested for HbS.

Welcome Laurasega.

Welcome JLH.

Welcome Abber.

I assumed the clerical side of things had already been checked.

Welcome M00t.

Welcome Muhammad Adamu.

Welcome S080jxh.

If the antibody was weak, it could be that there was a combination of a dilution effect from the plasma transfusion and associated IV fluids, but also adsorption of the weak and diluted antibody in vivo by the unit that was K Positive. If the patient has survived the trauma that brought him/her into the ER in the first place,you can probably expect a bounce back in titre within a couple of days, as the "excess" liquid will be excreted, and the immune system will "gear up" after the boost given by the K Positive unit. Mind you, sometimes, if the patient is bleeding profusely, the immune system seems to "shut down", in terms of being boosted.

I can't say that I am in the least surprised about this, given the patient's ethnicity. There is a frequency of the D antigen of 99% in most Asian populations.

While I would agree with you that no antibodies within the Duffy Blood Group System are well known for causing clinically significant HDFN, and repeating what I said above, that I have grave doubts as to this being such a case, the fact that you have not seen one does not mean that such things do not occur. I would cite Goodrick MJ, Hadley AG, Poole G. Haemolytic disease of the fetus and newborn due to anti-Fya and the potential clinical value of Duffy genotyping in pregnancies at risk. Transfusion Medicine 1997; 7: 301-304 (doi: 10.1046/j.1365-3148.1997.d01-38x), and indeed there has been a report of a "blocking" anti-Fya (which I should have remembered, not least because four of the six authors are personal friends!), namely Lee E, Cantwell C, Muyibi KO, Modasia R, Rowley M, New H. Blocking phenomenon occurs with murine monoclonal antibodies (anti-Fya) in a neonate with a positive direct antiglobulin test due to maternal anti-Fya. Blood Transfusion 2015; 13: 672-674 (doi: 10.2450/2015.0232-14). I would query your choice of words with regard to, "Gel card methods do funny things sometimes." I would rather like to know exactly what you mean.

Welcome Chris McCarty.

Why would the red cells of an individual who is Jk(a-b-) not react with Ulex europeaus?

Yes, the transfused red cells would eventually become the same Lewis type as the recipient. This has been known for some time, see Sneath JS, Sneath PHA. Adsorption of blood-group substances from serum on to red cells. Brit med Bull 1959; 15: 154-157, and Needs ME, McCarthy DM, Barratt AJ. ABH and Lewis antigen and antibody expression after bone marrow transplantation. Acta Haemat 1987; 78: 13-16. Not only in theory would there be no problems giving the rest of the first unit (as long as it is given relatively quickly after the first few mL, but it has been shown to be safe in practice. However, of course, the immune system will continue to produce anti-Lea, and so this "protection" will only last for a finite time.

What you are identifying is almost certainly a strong anti-H in an Oh individual. However, if the individual requires a transfusion, you will need to perform differential allo-adsorption (or something similar) to identify any other underlying clinically significant atypical antibodies (you can ignore any underlying Lewis antibodies, which are commonly also present).

Welcome Labhullu.

Looks like it could be an Oh individual. Try testing the red cells of the patient with Ulex europeaus.

It could also be that insufficient RhIg was given in the first place. How should I put this, umm, not all women are of the same size, and this makes a difference.

Anti-Lea CAN be clinically significant, but it is very rare for it to so be, and it tends to be self-limiting. For it to be clinically significant it has to be IgG and/or complement activating, and it is self limiting because, of course, the Lewis antigens are soluble. This means that they will be in any plasma remaining on the red cells in the unit, and these soluble antigens will inhibit the patient's anti-Lea in vivo. You can usually continue to transfuse the same unit that caused the problem after a while, with no further problems. MIND YOU, you have to be ABSOLUTELY CERTAIN that it was anti-Lea that caused the reaction in the first place!

Actually, you are quite right; there would have to be signs of HDFN - so forget the idea of a blocking antibody. I was letting my imagination run away with me. SORRY - silly idea!

I've had another thought about the baby's Fy(a) type being 1+, even though the control was 4+. It could be that the maternal anti-Fya was strong enough to be a blocking antibody. I have grave doubts about this, as blocking is rare, and I have never heard of a blocking anti-Fya, but there is a first time for everything!

Welcome Amanda Morris.