Malcolm Needs

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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.

No Mabel.  As always, Geoff is ABSOLUTELY right (and I would NEVER, in any case, go against one of the world's GREATEST in terms of Blood Group Serology).  Thank you also for your kind words, and I totally agree with your conclusion.

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.

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.

Thanks for your input.  I was hoping you might respond.
The Daniels book says that "No case of HDFN caused by anti-Lua or -Lub and requiring any treatment other than phototherapy is reported, although raised bilirubin or a positive DAT may be detected."  Does this description equal "clinical significant HDFN" by your definition or is there newer information on more severe HDFN from these since Daniels published the 3rd edition?  My thought is that, if there is no evidence of any case needing any early intervention, then there is no point in running titers to determine when to begin early intervention.
 

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Ha ha! Good thing I retired then

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.

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.

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.

Sounds like total rubbish from both a clinical and scientific viewpoint. Another instance how the administrative/legal model of reality is undermining civilization :).

We also inculed documents owner documents authorised by and effective date. 

I agree with Malcolm. I would dig as deep as possible to find that antibody history. If none can be found, I would do AHG crossmatches. If it was a frequent antibody, the titers should rise to detectable levels soon.

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".

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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!
 

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!
 

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!
 

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!