Bb_in_the_rain

Thanks for that - another EXCELLENT post.
I would say that not all cases of Weak D Type 1 with an allo-anti-D have been published.  I found one myself, and sent it to the IBGRL for confirmation.  It was confirmed and so I asked Joyce Poole if I should publish it as a case study, and she said no, because it wasn't new (the patient ws - the situation wasn't).

A powerpoint slide from 2018 AABB case presentation by Woo JS, et al. included a page of reported anti-D cases (see attached picture) So there would be 7 total cases of anti-D production in Weak D type 1,2, and 3,  including the case that was presented. The authors also have footnote that some of these anti-D has both auto- and allo- antibody characteristics. 

Since we have capability for molecular tests in this lab, we would refer to molecular testing for the following populations, (if D typing is <2+)
2) Women with child-bearing potentials
3) Potential transplant recipients
If you do not have molecular testing capability, I suppose you can call them D- (to be conservative) 
For the following population of patients, we interpret any positive reaction as D+ (if the DAT is negative) 
1) Males (<18 year old)  (exception  is our local Children's Hospital) 
2) Female with no child bearing potential 
3) blood or organ donors 
 
 
 
 
 

That will be my assumption as well. When I read up "Olsson M, et al. The Fyx phenotype is associated with a missense mutation in the Fyb allele Preductin Arg89Cys in Duffy glycoprotein.", authors explictly did not mentioned that individuals with Fya/Fyx does not produce anti-Fyb. 
That lead me to second guess myself and look for case reports but could not find any. 

Thanks for your advice. We often see neg DAT results with ABO HDFN in our work.( Because the A B antigens on the newborn red cells are weak )
You are right that I need an eluation result to support the HDFN .
As to anti-A1, we got 3 pos with A cells and 3 neg results with O cells. 
And yes, maybe due to infection the baby's cells can be polyagglutinatable, just cannot interfere with the plasma reaction with donors and screen cells.
 
 

Pity.  Correct nomenclature is vital to universal understanding.  This is why the ISBT has so many working parties!

That may be because she missed the 4th year of college where she has to start thinking about what to do after she finish school and real life situations. 

But we can pass SBB without brushing up on terminology. This is a different beast lol 

I just answered this question.


My Score PASS  

Once, as I was trying to help a student analyze a problem, she commented that she had had three years of college and I was the first person who had asked her to think! I suspect that's the norm.

I think it develops with experience.   Our older peers said the same thing about us. 

I try to scare them a bit...

I think that this would very much depend upon whether the red cells are from a donor or a recipient.  In the UK, for example, the anti-D reagents used in hospital laboratories, where they are testing (almost exclusively) patients, are designed not to detect Partial DVI, whereas those used in the NHSBT for donors and, to a certain extent, some of the reagents used in the Reference Laboratories are designed specifically to detect Partial DVI.  This means that an individual could be designated as D Positive as a donor, and D Negative as a recipient.  This would take a bit of explaining to the individual involved and, very often, to the doctor looking after the individual if they were not too familiar with transfusion.

I would be amazed if manufacturers would make such a direction, because it is unlikely that all anti-D reagents are guaranteed to detect ALL partial D types (notably the DEL types) but WILL detect ALL Partial DIII type individuals, which can, and often do produce an allo-anti-D.
I would be very confident to defend my own policy to a knowledgeable inspector, although I HOPE such an inspector would be knowledgeable enough NOT to ask about this in the first place!  The attached diagram is of Partial DVI Type 1 (copied from a diagram by Geoff Daniels).
Partial DVI Type 1.pptx

dothandar, an excellent post if I may say so (although I don't absolutely agree 100% with the terminology you use).
I agree that Weak D Types 1, 2 and 3 are to be regarded as D Positive, if the following two papers are to be followed - which I think they should (Daniels G.  Variants of RhD – current testing and clinical consequences.  British Journal of Haematology 2013; 161: 461-470 and Sandler SG, Flegel WA, Westhoff CM, Denomme GA, Delaney M, Keller MA, Johnson ST, Katz L, Queenan JT, Vassallo RR, Simon CD.  It’s time to phase in RHD genotyping for patients with a serological weak D phenotype.  Transfusion 2015; 55: 680-689).  However, as individuals of all three weak D types have, very, very rarely produced allo-anti-D (see Daniels G.  Human Blood Groups.  3rd edition, 2013, Wiley-Blackwell), they could all be put into your computer as WKDV.
Sorry, I am mucking you about - it really is an excellent post!

I completely agree with you with Weak D Type 1, 2 and 3. I think there are more than 3 cases of allo-anti-D so far. I am questioning the approach to give D+ blood to these patients as well (personally opinion, I know it may be an ongoing debate). Let me look up the case reports of anti-D in Weak D Type 1,2,or 3 to get back to you. I have a feeling that 3 is a bit too little. 
My other question is whether to look for other D variants when Weak D type 1,2,or 3 were detected in individuals of African origin as they may have other additional variants that can potentially lead to production of anti-D. 
I am very glad that you brought up these cases of anti-D in Weak D type 1,2 or 3. It truely is a great opportunity for further discussion. 
I admit that I can be neglectful when it comes to terminologies (which my mentors will not be happy about). I would really appreciate it if you would take the time to point our my terminology errors since it is something that I am trying to improve on. I am the type of person that constantly need to be nudged when it comes go terminology. (yes, one of those blood bankers!!!)
 

In this reference laboratory, either reference lab or submitting hospital decide whether to test RHD molecular or not. The RHD geno here is not by HEA beadchip but by other in-house methods. For the purpose of simplicity for our transfusion services staff, we translated the RHD results in terms of potential to produce anti-D and code them in as Antigens in our LIS. If RhD negative blood is warranted, we post D* as antibody (communicated to staffs as "give D- but patient has not make anti-D), so that LIS will stop us from issuing D+ units.
For patients with weak D type1, type2 or type 3, we used the codes WKD1, WKD2, WKD3 as antigens.
For patients with RHD variants that has potential to make anti-D. we used the code WKDV as antigens. We also put in predicted RHD variant in patient's comment (for example RHD*DAR or weakD 4.2.1 etc) Also post D* in antibody profile so LIS will stop the tech from issuing D+ units. 
For patients with RHD variant in heterozygote expression but also has normal D gene- we do not post anything in antigen or antibody profile. However we free text the predict allele in the patient's comment. For example, "Genomic RHD testing indicates a normal D allele with RHD* DAR1.2. (I suppose posting other terminology. like weakD 4.2.2 instead of allele name will be fine too) 
Hope it is helpful

The Blood Center we used does not label with historic antigen types, only confirmed. They do however put them in a spread sheet which gets sent to us. If we need a particular antigen we scan the spread sheet, find the unit/s we need and antigen type them ourselves

I am just wondering if anybody (any Blood Centers) has been labeling units with historical antigen typings since 2017 FDA guidance came out. For those who are doing these, I am also curious to see what kind of processes you have in place and which antigens you are labeling using historical antigen typing. *FDA guidance document attached* 
UCM534978.pdf

Wow Congratulation. Very well deserved. You have help educate not only your local blood bankers but also from those all around the globe. What an honor! 

During the serology workshop in recent AABB meeting, there was a presention from NYBC where HU5F9 clone was adsorbed out with red cells (3 cells /differential adsorption) was performed to mitigate this problem. There was also an abstract poster where HU5F9 clone was adsorbed out with platelet. Have you tried any of these adsorption methods on ALX 148? 
Let me try to find the hand out from the workshop and platelet adsorption abstract to see if I can scan it to here. 

Here is to the awkward moment when you go on blood bank talk webpage from your work computer, made the sound of broken glass, your coworkers turn around, gave you concerned look and asked "are you ok? was anything broken?": Happy Holiday! 

Here is to the awkward moment when you go on blood bank talk webpage from your work computer, made the sound of broken glass, your coworkers turn around, gave you concerned look and asked "are you ok? was anything broken?": Happy Holiday! 

In addition to the scenario that Yan has describe above, I would like to add awarm autoantibody, where the antibody is saturated on the patient's own cells but has not "spill" into the plasma, therefore DAT and autocontrol may be positive but non-reactive with reagent red cells. 

Here is to the awkward moment when you go on blood bank talk webpage from your work computer, made the sound of broken glass, your coworkers turn around, gave you concerned look and asked "are you ok? was anything broken?": Happy Holiday! 

In addition to the scenario that Yan has describe above, I would like to add awarm autoantibody, where the antibody is saturated on the patient's own cells but has not "spill" into the plasma, therefore DAT and autocontrol may be positive but non-reactive with reagent red cells.