galvania

I would just be a bit suspicious if say there was a + reaction with A1 cells and 4+ with B cells in an apparent group O - or vice versa; or very weak reactions in a young healthy adult.....a bit of common sense required, that's all

I would just be a bit suspicious if say there was a + reaction with A1 cells and 4+ with B cells in an apparent group O - or vice versa; or very weak reactions in a young healthy adult.....a bit of common sense required, that's all

I would just be a bit suspicious if say there was a + reaction with A1 cells and 4+ with B cells in an apparent group O - or vice versa; or very weak reactions in a young healthy adult.....a bit of common sense required, that's all

of course it could just simply be that the hospital lab made an error grouping it as a false positive.  As this is a question designed for new students, I doubt whether the level of scientific understanding required is very high at this stage.  It would depend what theory the students had done up until the point that the question was set

or mum is a surrogate
or baby is the result of an ivf with external donors

 

I would treated the patient's own red cells with papain or ficin (whichever is used by the manufacturer to make their enzyme treated red cells), and then test them against autologous plasma.  My guess (and from this far away, it is just a guess) is that they will be positive.
I think that there is a "cold" reacting auto-antibody there.
I would also suggest performing an IAT panel in tubes, bringing the reactants to 37oC before mixing them, and using isotonic saline, rather than LISS as the red cell diluent, and then washing the tests in pre-warmed isotonic saline.  This should show if there are any underlying clinically significant alloantibodies.

I agree that the difference between cisAB and B (A) is serological and divergent. They coulding be one, but they respect the names given by the authors. I do not think that the ABO * cisAB.05 and ABO * BA.06 alleles are different. It must have been an ISBT mistake!
See a summary I made in 2019.
In general, the phenotype cisAB presents normal expression of antigen A, but similarly to phenotype A2, and weak expression of antigen B. On the other hand, B(A) presents a very weak expression of antigen A, but a normal expression of B.(1)
    The rare phenotype cisAB was first described in a case of mother AB with child O.(2) Its authors suggested that this phenotype was formed by the interaction of two genes, one A2 gene and another atypical B gene, located in the same locus. However, with the molecular characterization of the cisAB-1 allele (ABO*cisAB.01), it was observed that a sequence of the ABO*A1.02 allele containing an additional mutation at position 803G>C (Gly268Ala) was capable of synthesizing a GT with mixed activity. The cisAB-1 allele is more common in Asian populations and considering the four positions that differentiate alleles A and B, it can be described as AAAB.(3) In a study of 16 Korean blood donors heterozygous for the ABO*cisAB.01 allele, it was demonstrated that both GTA and GTB have clearly decreased activity. GTA activity was 29% of GTB was 27% compared to wild GTA encoded by the A1 allele. (4) 
    Phenotype B(A) was first detected when monoclonal ABO reagents became commercially available. This phenotype exhibits normal levels of antigen B and very low levels of antigen A in tests with some anti-A monoclonal reagents. (1) The GT of this phenotype has the ability to produce normal levels of antigen B, but also use The UDP-GalNAc as substrate to produce detectable levels of antigen A.
    The B(A) alleles are variants of allele B and the first of them (ABO*BA.01) was identified by Yamamoto and collaborators. (5) This allele is commonly referred to as BABB due to the aa of position 235 being the same as consensus A1. The second allele B(A) (ABO*BA.02) has the aa sequence of allele B, being referred to as BBBB, but contains an additional mutation at position 700C>G (Pro234Ala) which is close to aa 703, one of the four that differentiate the A allele from B.(6,7) 
    By the way, a normal GTB encoded by the consensus B allele has the ability to synthesize minimal amounts of antigen A which are detectable by some anti-A reagents. As well, GTA encoded by the A consensus alleles can also synthesize minimal amounts of antigen B, which are detectable by some anti-B reagents. These reagents were considered inappropriate for the ABO phenotyping routine,(8) for example, the anti-B monoclonal antibody (BS-85), reported by Voak et al. (9)
1. Daniels G. Human blood groups: Introduction. Oxford, UK: Wiley-Blackwell2013.
2. Seyfried H, Walewska I, Werblinska B. Unusual inheritance of ABO group in a family with weak B antigens. Vox Sang. 1964;9:268-77.
3. Yamamoto F, McNeill PD, Kominato Y, Yamamoto M, Hakomori S, Ishimoto S, et al. Molecular genetic analysis of the ABO blood group system: 2. cis-AB alleles. Vox Sang. 1993;64(2):120-3.
4. Cho D, Shin MG, Yazer MH, Kee SJ, Shin JH, Suh SP, et al. The genetic and phenotypic basis of blood group A subtypes in Koreans. Transfus Med. 2005;15(4):329-34.
5. Yamamoto F, McNeill PD, Yamamoto M, Hakomori S, Harris T. Molecular genetic analysis of the ABO blood group system: 3. A(X) and B(A) alleles. Vox Sang. 1993;64(3):171-4.
6. Haslam DB, Baenziger JU. Expression cloning of Forssman glycolipid synthetase: a novel member of the histo-blood group ABO gene family. Proc Natl Acad Sci U S A. 1996;93(20):10697-702.
7.  Yu LC, Lee HL, Chan YS, Lin M. The molecular basis for the B(A) allele: an amino acid alteration in the human histoblood group B alpha-(1,3)-galactosyltransferase increases its intrinsic alpha-(1,3)-N-acetylgalactosaminyltransferase activity. Biochem Biophys Res Commun. 1999;262(2):487-93.
8. Goldstein J, Lenny L, Davies D, Voak D. Further evidence for the presence of A antigen on group B erythrocytes through the use of specific exoglycosidases. Vox Sang. 1989;57(2):142-6.
9. Voak D, Sonneborn H, Yates A. The A1 (B) phenomenon: a monoclonal anti-B (BS-85) demonstrates low levels of B determinants on A1 red cells. Transfus Med. 1992;2(2):119-27.
 

or mum is a surrogate
or baby is the result of an ivf with external donors

 

or mum is a surrogate
or baby is the result of an ivf with external donors

 

or mum is a surrogate
or baby is the result of an ivf with external donors

 

or mum is a surrogate
or baby is the result of an ivf with external donors

 

"Sure it could happen ,,, and here's how... one of the parents perhaps has the Bombay phenotype" 

Thank you Malcolm.  Our prenatal titer procedure calls for reading microscopic solely for the purpose of scoring, but I guess there isn't an associated score .  Looks like the procedure should be updated 

Macroscopic every time.

to be fair techniques in the early 80s were not what they are today, neither for blood grouping nor for antibody screening/identification.  Methods were not standardised.  The number of drops of serum (almost always serum) to the amount of red cells could vary from 2:1 to 8:1.  The concentration of the red cells could be anything from about 2% to almost 10% - and often pooled. And pooling was one of the main reason for checking under the microscope.  Incubation time varied too - often depending on the length of your coffee break or lunch break.  LISS was in its infancy.  Washing was done by hand or with a 'Coombs washer' - 3 or 4 washes, with or without albumin.  So perhaps not surprising that people were not too confident in their visual results.  Much less knowledge then too about what was and what was not clinically significant.  (I can remember when we treated cold anti-A1 as clinically significant)
Thankfully since those dark ages things have improved massively - but sometimes some of the old habits stick - like using a microscope to read apparently negative results.  The practice lives on  (in some places) but the reasons for that practice died out long ago

When we first started using Gel, my techs would point out the shadows or 'jumpies' as they called them. 
I'd suggest 'Run the screen again using maxtime.'  If they still saw the shadows, I'd just let them run a panel (maxtime) and go crazy with the results.  After a while we all learned to ignore those reactions. 
Keep in mind, there are always a certain percent of any given cell population (especially stored reagent cells) that are just not going to make it smoothly to the very bottom solely because of steric hindrance (broken, aged, crenated, tagged for destruction, etc.).

to be fair techniques in the early 80s were not what they are today, neither for blood grouping nor for antibody screening/identification.  Methods were not standardised.  The number of drops of serum (almost always serum) to the amount of red cells could vary from 2:1 to 8:1.  The concentration of the red cells could be anything from about 2% to almost 10% - and often pooled. And pooling was one of the main reason for checking under the microscope.  Incubation time varied too - often depending on the length of your coffee break or lunch break.  LISS was in its infancy.  Washing was done by hand or with a 'Coombs washer' - 3 or 4 washes, with or without albumin.  So perhaps not surprising that people were not too confident in their visual results.  Much less knowledge then too about what was and what was not clinically significant.  (I can remember when we treated cold anti-A1 as clinically significant)
Thankfully since those dark ages things have improved massively - but sometimes some of the old habits stick - like using a microscope to read apparently negative results.  The practice lives on  (in some places) but the reasons for that practice died out long ago

to be fair techniques in the early 80s were not what they are today, neither for blood grouping nor for antibody screening/identification.  Methods were not standardised.  The number of drops of serum (almost always serum) to the amount of red cells could vary from 2:1 to 8:1.  The concentration of the red cells could be anything from about 2% to almost 10% - and often pooled. And pooling was one of the main reason for checking under the microscope.  Incubation time varied too - often depending on the length of your coffee break or lunch break.  LISS was in its infancy.  Washing was done by hand or with a 'Coombs washer' - 3 or 4 washes, with or without albumin.  So perhaps not surprising that people were not too confident in their visual results.  Much less knowledge then too about what was and what was not clinically significant.  (I can remember when we treated cold anti-A1 as clinically significant)
Thankfully since those dark ages things have improved massively - but sometimes some of the old habits stick - like using a microscope to read apparently negative results.  The practice lives on  (in some places) but the reasons for that practice died out long ago

to be fair techniques in the early 80s were not what they are today, neither for blood grouping nor for antibody screening/identification.  Methods were not standardised.  The number of drops of serum (almost always serum) to the amount of red cells could vary from 2:1 to 8:1.  The concentration of the red cells could be anything from about 2% to almost 10% - and often pooled. And pooling was one of the main reason for checking under the microscope.  Incubation time varied too - often depending on the length of your coffee break or lunch break.  LISS was in its infancy.  Washing was done by hand or with a 'Coombs washer' - 3 or 4 washes, with or without albumin.  So perhaps not surprising that people were not too confident in their visual results.  Much less knowledge then too about what was and what was not clinically significant.  (I can remember when we treated cold anti-A1 as clinically significant)
Thankfully since those dark ages things have improved massively - but sometimes some of the old habits stick - like using a microscope to read apparently negative results.  The practice lives on  (in some places) but the reasons for that practice died out long ago

to be fair techniques in the early 80s were not what they are today, neither for blood grouping nor for antibody screening/identification.  Methods were not standardised.  The number of drops of serum (almost always serum) to the amount of red cells could vary from 2:1 to 8:1.  The concentration of the red cells could be anything from about 2% to almost 10% - and often pooled. And pooling was one of the main reason for checking under the microscope.  Incubation time varied too - often depending on the length of your coffee break or lunch break.  LISS was in its infancy.  Washing was done by hand or with a 'Coombs washer' - 3 or 4 washes, with or without albumin.  So perhaps not surprising that people were not too confident in their visual results.  Much less knowledge then too about what was and what was not clinically significant.  (I can remember when we treated cold anti-A1 as clinically significant)
Thankfully since those dark ages things have improved massively - but sometimes some of the old habits stick - like using a microscope to read apparently negative results.  The practice lives on  (in some places) but the reasons for that practice died out long ago

to be fair techniques in the early 80s were not what they are today, neither for blood grouping nor for antibody screening/identification.  Methods were not standardised.  The number of drops of serum (almost always serum) to the amount of red cells could vary from 2:1 to 8:1.  The concentration of the red cells could be anything from about 2% to almost 10% - and often pooled. And pooling was one of the main reason for checking under the microscope.  Incubation time varied too - often depending on the length of your coffee break or lunch break.  LISS was in its infancy.  Washing was done by hand or with a 'Coombs washer' - 3 or 4 washes, with or without albumin.  So perhaps not surprising that people were not too confident in their visual results.  Much less knowledge then too about what was and what was not clinically significant.  (I can remember when we treated cold anti-A1 as clinically significant)
Thankfully since those dark ages things have improved massively - but sometimes some of the old habits stick - like using a microscope to read apparently negative results.  The practice lives on  (in some places) but the reasons for that practice died out long ago

In my opinion, this very much depends upon the underlying pathology.  For example, if the patient has an auto-immune haemolytic anaemia, the chances are very strong that the DAT will be positive before as well as after the transfusion, and that any eluate will be positive with all red cells tested (of normal type).  The chances of detecting a new antibody specificity on the DAT positive red cells under these circumstances is disappearingly small.
Therefore, if the sample is sent to a reference laboratory on a regular basis, your manager will be 1) showing a degree of ignorance that should be surprising, 2) will be upsetting the staff of the reference laboratory, as most have enough to do, without having to perform extra, unnecessary work, and 3) as you are in the UK, will be wasting the tax payer's money (and, as a UK tax payer, I feel very strongly about this).
If, on the other hand, the positive DAT is new, then a reference laboratory would be delighted to help out.
Of course, what your manager could do is to buy his/her own laboratory an elution kit, and train his/her staff to use it!!!!!!!!!!!!!!!!  This may bring the cost of the kits to meaningful results ratio to the overall pathology manager, which could be of interest!

of course it could just simply be that the hospital lab made an error grouping it as a false positive.  As this is a question designed for new students, I doubt whether the level of scientific understanding required is very high at this stage.  It would depend what theory the students had done up until the point that the question was set

For tube testing using the "uniform procedure tube method" that CAP suggests, they reported the following results: 333 participants, mode 64, consensus range 16 to 256.  For Gel testing "uniform procedure gel method", 138 participants, mode 256, consensus range 64 to 1024. 
Sorry but that range of results is just HUGE regardless of method. FIVE dilutions difference.   Something tells me there is no standardisation in either method.  Things like dilution medium can make a big difference as can the choice of cell phenotype used to carry out the titre.  I hope individual labs are not getting that level of range when they repeat a titre!
I also have never heard of CRP affecting results in gel; and I fail to see by what mechanism it could.  I have, on the other hand, heard that transfusion during a period when the patient has a high CRP can be more likely to induce de novo antibody formation

I would just like to add one 'grain of salt' to this debate.  You cannot detect all D variants - whether D weaks or partial Ds by serological methods alone. Neither D weaks or Partial Ds behave in a way that allow one to say that all D weaks  or partial Ds react with such and such a strength.  You will always miss some.  You will miss some D+ donors because their D antigen is so weak that it is not detected by even the most sensitive of routine serological tests - or because despite using at least two different monoclonals the donor has an extremely unusual variant that is detected by neither.  You will miss some 'D-neg' patients  because they have sufficiently large numbers of D-antigen sites that they give a normal reaction with the anti-D reagents used.  Follow the manufacturer's instructions for the reagent and method used and you will detect as many as you can hope to detect.  And before you shoot the manufacturers because their reagent/instrument gave a 4+ reaction with a partial D known to have 10'000 D-antigen sites per red cell, and discovered because the lady made an anti-D and she is pregnant - please take a minute to think about the theory behind the serology.  Maybe in years to come there will be a foolproof routine method for catching every single one……...