We have a patient who received many units of group/type specific red cells in Jan. of this year. At that time, his antibody screen was negative. His group and type is A, Rh positive using monoclonal typing reagents. The anti-D reactions have been 2+ and 3+.

His current specimen shows an anti-E in the plasma and a panagglutinin in the eluate tested in gel, with stronger reactions in the D+ cells. His eluate tested in tube shows a clear anti-D pattern.

Could this be a D variant? Auto-anti-D? Should he get Rh negative red cells?

Thanks!

 

If the patient HAS NOT been transfused since January, all of the red cells in the circulation should be his own.

 

As the anti-D can be eluted from his own red cells, it seems far more likely to me that this is an auto-anti-D, than an allo-anti-D formed by a patient with a Partial or Weak D type.

 

I take it that he has now got a positive DAT (?), otherwise why perform an eluate?  If this is the case, this is even more reason to support the theory of an auto-anti-D.

 

As gel is more sensitive than tube, and you are getting a panagglutinin in gel, but an anti-D in tube, it could even be that the actual specificity of the auto-antibody could be a transient auto-anti-LW, rather than anti-D.  If you can, try testing some group O or group A, rr cord cells against the eluate by tube technique.  If these are positive, then the theory of auto-anti-LW is much more likely.

 

What is his underlying pathology, by the way?

The patient's admitting diagnosis was septicemia but he acutally had heart surgery. I don't know the intervening issues or procedures. In Jan. he was in the medical ICU with some sort of respiratory issue. I only know that he was on a pulmonology service.

A blood banker friend of mine suggested that I treat the patient's cells with EGA and then run the eluate and the plasma against the treated cells to determine if the antibody was auto or allo.

I will try running against cord cells too, if I can find some with the suggested phenotype. We don't keeps such things on hand. Thanks for the input.

Thanks for that kirkaw.

 

Presumably then, he had a transfusion during the heart surgery, and it is this transfusion that could have "brought on" the auto-antibody.  Petz and Garratty say in their book that transfusions can cause the production of auto-antibodies, or exacerbate the production of pre-existing auto-antibodies.

 

This is another reason why transfusions are always a sort of risk/benefit analysis.

 

What is EGA, by the way?  I am not familiar with this particular acronym - although that does not mean that I may do the same under a different title!!!!!!!!!!!!!!

EGA is Ethylene/Glycine Acid and is used instead of Chloroquine treatment.

_{EGA is nice but in this case it will not help. EGA can also be used to remove HLA antigens (and Kell). The procedure takes more than 10 minutes (instead of 2 hours when you use Chloroquine)}

 

_{In case of allo antibodies against donors cells, the EGA will remove the antibodies. When you then test the eluate again with the patient cells (that contains donor cells) will be reactive. In that case you have to collect/concentrate reticulocytes and test the eluate with those, that is a real autocontrol.}

 

_{As Malcolm mentioned, If transfusion is more the 3 months ago, it must be auto antibodies.}

Is your patient African American?  We have several sickle patients and multiparous women with Anti D.

Another possible scenario - the cardiac surgery was actually a transplant of a D+ heart and the patient really is a partial D (weak reactions present with anti-D)and has made allo-antibodies against the D+ heart?????

I do not remember the ethnicity of this patient, but it very well could've been an African American.

As for the cardiac surgery being a heart transplant, the answer is no. We do not do transplants here.

The LW can also be confirmed after treatment with DTT.

I agree with Malcolm Needs, I think this scenario an auto-anti-LW or auto-anti-D is more likely.