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Malcolm Needs

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Posts posted by Malcolm Needs

  1. I wouldn't bother, to be honest.

    Apart from the fact that the Lutheran antigens vary in strength of expression, making it difficult to ensure that the recorded titres would "match up" one to another, but the expression of the Lutheran antigens on foetal and cord erythrocytes is known to be weak.  On top of that, of course, there is the problem of finding a regular source of adult erythrocytes with heterozygous expression.

    In addition, anti-Lua and anti-Lub can be either IgG or IgM but are more commonly IgM.  It might be worth your while treating the maternal plasma/serum with a reducing agent such as 0.01M dithiothreitol, 2-mercaptoethanol or ZZAP to see how much, if any, IgG is present.

    Even if the antibodies are IgG, they are thought to be adsorbed on to foetal Lutheran glycoprotein on the placental tissue.

    Lastly, as you so rightly say, clinically significant HDFN caused by anti-Lub is incredibly rare, and so, all in all, you could be giving yourself an awful lot of work for very little return.  If you do decide to test the maternal plasma/serum with reducing agent, and you find that there is an element of IgG present, it might be worthwhile just performing a titre once, in order to see that you have not got one of these incredibly rare examples that might cause clinically significant HDFN, and, as lone as the titre isn't massive. I would rest easy.

    If you want, I can cite references to back up what I have written above, but I haven't done so straightaway, as actually finding some of these papers to read is equally hard work!!!!!!!!!!

    I hope that helps.

  2. In the UK, NHSBT stopped performing a DAT routinely on donor units some time ago (when I was still working).  If a unit was found to be DAT positive through, for example, an incompatible cross-match, and the unit was returned to the supplier, the unit was tested, and then discarded, and the hospital reimbursed.  If considered necessary, the donor's GP was informed.

    However, of course, it is almost certain that many DAT positive units were not discovered, and were transfused to a patient as a result of electronic issue.  I have NEVER heard of a patient having any serious clinical sequalae as a result of this practice.

  3. The simple answer is gagpinks, but this is the answer I have just received from my friend at the IBGRL (who shall remain anonymous for now).

    The question I put was as follows:

    "Sorry to bother you yet again, but I have had a query from a friend. I think I know the answer, but I wanted to check with an expert. If a pregnant lady has an allo-anti-D, can this affect cffDNA harvesting from the mother's circulation? I don't think it does unless the anti-D knocks out all of the foetal red cells. Best wishes from this bloody nuisance, Malcolm"

    Answer below.

    "Hi, that's right, anti-D makes no difference to the cffDNA test. The two biggest problems are false negatives due to insufficient RHD gene in the test sample and mums with a RHD gene (despite pheno typing as D-) leading to strong positive results. Take it easy."

    As I said, the friend will remain anonymous for now, but, suffice it to say, he/she is one of the people who do the test, so I think the answer can be trusted!

     

  4. This may not be easy/possible to do, but have you checked that the patient had not been given a very large dose of anti-D immunoglobulin during her first pregnancy?  It is not totally unknown for a woman to develop an allo-anti-D in her first pregnancy, although it is incredibly rare, but, if the patient had an abdominal trauma, she could well have been given a very large dose of anti-D immunoglobulin.

    This may explain why her antibody screen was negative at 12 weeks of gestation in her second pregnancy.

    There is also the (vague) possibility that the anti-D in the patient's circulation first pregnancy MAY have been a mis-identified anti-LW.

    I must confess that I am slightly at a loss as to why the 15 week sample could not be used for foetal RHD genotyping, leading to a prediction of the D antigen expression on the foetal red cells, unless all the foetal red cells had been cleared from the maternal circulation.  If this is the case, there are still other ways of obtaining foetal DNA (albeit more dangerous), such as foetal reticulocytes in the amniotic fluid.  If the "anti-D" is only "enzyme-reactive", it is true that it would be impossible to quantify, but it is also most unlikely to be clinically significant in terms of HDFN (but I wholeheartedly agree with you that it should be monitored throughout the pregnancy).

    I take it that the first pregnancy resulted in a successful delivery of a healthy baby?

  5. I would most strongly advise you to send a sample, possibly even multiple samples throughout the pregnancy, to a Reference Laboratory.

    As the patient is pregnant, there is the possibility that the Jk(a) antigen you are detecting is actually being expressed on the red cells of the foetus, and you are detecting it as a result of a foeto-maternal haemorrhage.  However, the Jk(a) antigen is not necessarily straight forward, as there are weakened forms of the antigen (and the Jk(b) antigen come to that) where there are amino acid substitutions remote from the site usually associated with the Jk(a) and Jk(b) antigens (280 of the mature protein).

    In addition though, you have, obviously, to consider the health of the unborn baby who, even if the antibody does turn out to be a maternal auto-anti-Jka, may cause haemolytic disease of the foetus and newborn, albeit this will usually be be very mild.

    I attach a PowerPoint which may, or may not help you in your decision to send a sample to your local Reference Laboratory (also tell them the ethnicity of the patient).
     

    Interesting case - please keep us informed.

    In Depth Lecture on The Kidd Blood Group System.pptx

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