Malcolm Needs

Certainly in the UK, if they are known to be sickle cell positive, whether trait or disease, are supposed to have HbS Negative blood.

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).