lab217

We allow it, unless there is a mixed-field reaction with any of the antisera (except of course, a Lewis type, as these change drastically with pregnancy).

The report of auto C and e is coming from our reference lab.  The reference lab only added that their facility does not "follow" prenatal patients with autoantibodies. 
 
  In 2011 her antibody screen was negative, no DAT was performed. Her phenotype is R1r(C+E+c+e). She is caucasion and has not been transfused.  This is her second pregnancy. 
 
Could you give me a little more information regarding the two allos you mention.
 
Lastly, is there anything documented that you know of that I can reference regarding not needing to "follow/titer" prenatals with auto antibodies.
 
Malcolm, have I told you recently how awesome I think you are?  Your expertise is greatly appreciated!

The report of auto C and e is coming from our reference lab.  The reference lab only added that their facility does not "follow" prenatal patients with autoantibodies. 
 
  In 2011 her antibody screen was negative, no DAT was performed. Her phenotype is R1r(C+E+c+e). She is caucasion and has not been transfused.  This is her second pregnancy. 
 
Could you give me a little more information regarding the two allos you mention.
 
Lastly, is there anything documented that you know of that I can reference regarding not needing to "follow/titer" prenatals with auto antibodies.
 
Malcolm, have I told you recently how awesome I think you are?  Your expertise is greatly appreciated!

Malcolm, you are a wealth of knowledge and are greatly appreciated! Thank you, thank you.
 
Apologies in advance to your fellow employees, but I must say I would be glad to "put up" with your ego, any day!

Hi lab217,
 
First of all, thank you so much for your very kind words.
 
I am now happy that the antibodies are truly auto-antibodies, given both the lady's Rh phenotype and her ethnic origin, and I would agree with your Reference Laboratory that serial titrations during the pregnancy are not required.  The rational for saying this is in Petz LD, Garratty G.  Immune Hemolytic Anemias.  2nd edition, 2004, Churchill Livingstone, Chapter 9, pages 346-347.  Here, you will find reference to the fact that foetuses can be fatally affected in a pregnancy involving autoimmune haemolytic anaemia, BUT (and this is the important bit) these fatalities are due to the maternal Haemoglobin levels dropping to <60gL-1, and so there is a lack of oxygen transfer to the foetal red cells, rather than the auto-antibody causing a haemolytic crisis in the foetus.
 
When the maternal haemoglobin levels are controlled (by steroids, transfusions, etc, so that sufficient oxygen was getting to the foetal red cells) there was little, if any, evidence of a clinically significant episode of haemolytic disease of the foetus and newborn, beyond the fact that some babies had a positive direct antiglobulin test.
 
Turning to the two alloantibodies I mentioned.  Anti-Ce (also known as anti-Rh7 and anti-rhi - just to confuse matters!!!!!!!!) is a compound antibody that will only react with red cells expressing both the C and e antigens that have been encoded in the same haplotype (rather like anti-ce/anti-f, that will react with rr red cells [RHc and RHe genes in the cis position], but not with R1R2 red cells [RHc and RHe genes in the trans position]).  So, basically what I am saying is that, if a foetus has the phenotype of D+ C+ c+ E+ e+, if the baby's genotype is DCe/DcE, there is a chance that an anti-Ce could affect the baby, whereas, if the baby's genotype is DCE/dce, the baby will not be affected by a maternal anti-Ce.
 
The good news is that anti-Ce is usually only associated with very mild HDFN.
 
Anti-hrB (anti-Rh31) is an antibody that can be produced by individuals who have a variant of the e antigen (a variant that is, to all intents and purposes, only seen within the Black populations - hence the fact that I am comforted by the fact that your pregnant lady is Caucasian).  Anti-hrB mimics a mixture of anti-C and anti-e, with the anti-C-like element often showing as a stronger antibody than the anti-e-like element.  Again, anti-hrB is not usually associated with clinically significant HDFN.  However, there is another Rh antibody, again, normally only found in an individual from the Black populations, anti-HrB (anti-Rh34) that, when weak, or just developing, can mimic an anti-hrB.  Again, anti-HrB is usually associated with mild HDFN, although somewhere in the back of my mind, I seem to recall one case where the baby was severely affected, and required several transfusions (with washed and irradiated maternal blood, which was of the "wrong" ABO type, but the baby survived).  If I am correct, and I can find the reference, I will post this for you.
 
Anyway, I hope this post has served to help you in some way, rather than to confuse the issue further!
 
       

The report of auto C and e is coming from our reference lab.  The reference lab only added that their facility does not "follow" prenatal patients with autoantibodies. 
 
  In 2011 her antibody screen was negative, no DAT was performed. Her phenotype is R1r(C+E+c+e). She is caucasion and has not been transfused.  This is her second pregnancy. 
 
Could you give me a little more information regarding the two allos you mention.
 
Lastly, is there anything documented that you know of that I can reference regarding not needing to "follow/titer" prenatals with auto antibodies.
 
Malcolm, have I told you recently how awesome I think you are?  Your expertise is greatly appreciated!

Whilst there is general agreement that Malcolm is, indeed, awesome, those of us lucky enough to know him try not to tell him too often in case it goes to his head  

Dang!  I should have slipped in  "probably is an A1 individual".  (You are very alert for a Monday morning!)
 
 
Donna

Same as David.  

Actually, I have to disagree L106, as, if the anti-A1 being used is Dolichos biflorus, this lectin will also detect Tn activation and Cad polyagglutinability - both highly unlikely, but both possible.
 
Sorry!

No.  If the patient's red cells demonstrate a positive reaction when tested with Anti-A1 Lectin it indicates that the patient is an A1 individual (and there is no reason to test the patient's plasma against A2 cells.)

I only use the A1 lectin if I am dealing with a reverse grouping discrepany (grA backtypes as an O).

Certainly, in the UK, this is not, to say the least, a routine procedure.

Not quite sure what the DAT is adding to the mix.   I could see if you are using AHG antisera but even then, the negative control would not be negative.   A positive DAT may also interfere with RT antisera (rare but possible) but then again, the negative control would not be negative. If controls work you should be good to go. 

We do a visual inspection and use positive control (antisera matching the antigen in question) and negative control (6% albumin) per panel cell. This topic has come up a few times recently due to some of our more involved ABIDs.