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B subtypes


klsmith

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Hi Blood Bankers!

So I have recently come across information about B subtypes. The literature that I was reading talked about B3, Bx, Bm, and Bel. I currently know next to nothing about these subtypes, and I am looking to know more about them! (Malcolm, I am especially counting on your expertise here, "hint, hint!") Anyway, if anyone has any info to offer, I would so appreciate it!

Thank you!

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Malcolm,

Here is the web address that I was reading the article on: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-84842016000300264

I was originally trying look up AML and the potential loss of blood group antigens on RBC's that could be associated with it, and I stumbled across this information. I had initially attempted to share my find with my best and most knowledgeable co-worker in my Blood Bank, but he was unable to access it through the web address. That being said, if you run into the same issue, then please let me know, and I can email the page to you, just please give me your email address.

 

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6 hours ago, klsmith said:

Malcolm,

Here is the web address that I was reading the article on: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-84842016000300264

I was originally trying look up AML and the potential loss of blood group antigens on RBC's that could be associated with it, and I stumbled across this information. I had initially attempted to share my find with my best and most knowledgeable co-worker in my Blood Bank, but he was unable to access it through the web address. That being said, if you run into the same issue, then please let me know, and I can email the page to you, just please give me your email address.

 

Hi Kelly,

Got it, and am printing it out.  I will then read it and, when I get a second today, I will get back to you.

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Okay, well, as you know from the paper, inherited weak B is rare, and the acquired weak B is even rarer.  This can be evidenced from the fact that in Race RR and Sanger R, Blood Groups in Man, 6th edition, Blackwell, 1975, only two pages of 659 are devoted to the weak B type, although Yamaguchi H, Okubo Y, Tanaka M.  A rare blood Bx analogous to Ax in a Japanese family.  Proc Jap Acad 1970; 46: 446-449 showed that the weak B type is more common amongst the populations of the Far East, than they are amongst other populations.  38 years later, Geoff Daniels, in Daniels G.  Human Blood Groups, 3rd edition, Wiley-Blackwell, 2013, still only devotes two and a half pages to weak forms of the B antigen.

This having been said, in Reid ME, Lomas-Francis C and Olsson ML.  The Blood Group Antigen FactsBook, 3rd edition, Academic Press, 2012, Martin Olsson (I presume, as he is famed for his work on the molecular study of ABO types), quotes eight different molecular backgrounds to B3, 33 different molecular backgrounds to Bx and Bm, and five different molecular backgrounds to Bel.  The overwhelming ethnicity of these individuals are from the Far East, although by no means all.

As described in the paper you provided to me, A and B antigens can weaken with certain underlying pathologies.  I have never seen this myself in a group B patient, but I did once in a group A patient with acute myeloid leukaemia, who also happened to be a Consultant Haematologist in a large London Teaching Hospital.  We were able to follow whether she was in remission or relapse from the strength of the expression of her A antigen.

It is not really known why this happens, although, as they point out in the paper you provided for me, it could be that the B transferase is altered by mutation, but, if this was the only explanation, when an individual goes into remission, it is doubtful if the mutation in the B transferase gene would resolve.  It is possible that the transferase loses its ability to attach D-galactose to all of the four (probably eight) carrier molecules.

We know that the A, B and H transferase enzymes are not working at their optimum at birth (which is why the expression of the A, B and H antigens are not at their strongest at this time of life - it is not until the age of three that the antigens are expressed at their full strength, and they can then weaken with extreme age).  However, the number of B antigen sites differs profoundly between a B adult (610,000 - 830,000) and an A1B adult (310,000 - 5650,000) (Economidou J, Hughes-Jones NC, Gardner B.  Quantitative measurements concerning A and B antigen sites.  Vox Sanguinis 1967; 12: 321-328).  This is because the A and the B transferase enzymes compete with one another for the carrier molecules.  This competitiveness can, sometimes, result in profound weakening of either the A or the B antigen on the red cells.

I hope this helps.  If not, get back to me.

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