Auto anti-G?

[Letty]

We have a 92 yr old patient who was transfused three units of blood 18 months ago.  She was recently re-admitted with infection and haematemesis when pre-transfusion testing revealed the presence of anti-Fya plus apparent anti-C+D (with positive autocontrol) in her plasma.  Her D group is weakly positive, so we duly referred samples to our reference centre to confirm her group and our suspicions of an anti-G (due to variations in reaction strength).  Her group has been reported as O RhD positive (Weak D) C-c+E+e+K+but the anti-G detected is reported to be Auto.  My question is, how can the reference centre determine whether the antibody is allo or auto? - Surely an allo anti-G will cross-react with the patient's own cells, leading to a positive auto and subsequent elution of the antibody from the patient red cells?  The reference centre failed to explain why the antibody must be an auto, despite being quizzed by ourselves and were absolutely adamant that it wasn't an allo anti-G.

Edited July 10, 2019 by Letty

[Malcolm Needs ☆]

My own questions would be, firstly, what on Earth are you doing identifying the RCI Laboratory concerned (poor form) and, secondly, what on Earth are they doing wasting public money by proving the presence of an anti-G in a 92-year-old patient, when knowing the exact specificity of the Rh antibody/antibodies in the patient's plasma will make no difference to what blood she will be given, should she require a transfusion?

[Letty]

Apologies, you are quite right, and i have edited my post.  Regardless of the ethics of performing the testing, i would still be interested to know how you can differentiate between the two.

[Malcolm Needs ☆]

Well, the easiest way is to type the patient's red cells with an anti-G.  I cannot imagine an RCI Laboratory that would not have an anti-G to hand.  Don't forget that, as long as the antibody is only used "in house", it does not have to be CE-marked.

Obviously, I don't know the individual case myself, but I would imagine that much of the work would have been performed using papain-treated red cells, as this would serve both to enhance the Rh antibody/antigen reaction, and to ablate the reaction between the anti-Fya and the Fy(a) antigen.  To do this, they would have to have treated the patient's own cells with papain (to act as a control), and it would be with these that the antibody could best be shown to be an auto.

Not all auto-antibodies cause a positive DAT, or can be detected in the auto by a traditional IAT (Sachs UJH, Roder L, Santoso S, Bein G.  Does a negative direct antiglobulin test exclude warm autoimmune haemolytic anaemia?  A prospective study of 504 cases.  British Journal of Haematology 2006; 132: 651-661), but it is routine these days for RCI Laboratories in NHSBT to test by IAT with untreated red cells, and IAT using papain-treated red cells, rather than by the use of papain-treated red cells in a "saline" column agglutination cassette.  Papain-IAT is much more sensitive, and gives crisper reactions.

As I say, I don't know for certain what they did, but I would be prepared to bet a modest amount that this was how the sample was tested, and the "auto" may well have been positive by papain-IAT, but the plasma may not have contained a panagglutinin.