Yanxia

But they do the test again ,and paralell with another specimen, the result is same, so I don't agree with you that the factor is antigen sites differ. Why you think anti-G make the result of anti-C was stronger than anti-D and why the baby was clinically unaffected? Thank you!

I don't think there is relationship between the binding and the clinical significance of the antibody. Some antibodies can bind to rbc but no ducuction of the cells' life span.

I don't agree with you.Mom's anti-A,anti-B or anti-AB can bound on the cells and the DAT is negative. We will do hot elution in this condition.

Thank you, Malcolm. I have another question : why not wash the RBC be transfused to neonatal and pediatric?

I think the gel technology is more sensitive , it is safer than the tube and liss method.

I remember if the patients have high level of potassium, the transfused RBC need to wash, is there something new to change this practice? Help is appreciated.

Chloroquine phosphate can eluate the antibodies and keep the cell's integrity.

What is Anti-fuju?

I remember have seen it in 15 edition of AABB technical mannual, but I am sorry it is not on my hands.

Is it the destroyed cells in the eluate?

I think this depend on how many blood have been transfused. And gene detect if a good approach.

Maybe you can change the reagent anti-A and anti-B or try to incubate Rituxan and other known O type cells in 37 degree C for 30 minutes, and then type it with the same reagent anti-A and anti-B, to see if the reagent have something reacted with the rituxan on the red cells.

Thank you, David. I am the poster. I wondered what will happen when the patient transfused under daylight. Sorry for my adamancy.

AHG reagent is IgG antibodies have two legs only, the principle it can detect the IgG or complement on the red cells is when the two legs link two red cells together, we can see the agglutination. But when the time past or respin the IgG antibodies in the AHG reagent may dissociated from the cells and rejoin, two legs of an antibody joined ith one cell, then the agglutination is disappear. This theory can't interprete the complement DAT testing.

I agree with L106 about the autocontrol. And what about the reverse group result? Rituxan is a kind of antibody preparation, maybe it can interfere the ABO group testing .

The DAT positive patient, some include antibodies have real specificity and others are mimicking antibodies. And the mimicking antibodies can be adsorbed by the antigen positive and negative cells( all or partial). It can be divided into two kind of antibodies, one is the antigen present on the patient's cells ,the other is the antigen is not present on the patient's cells. I think this patient maybe have the later mimicking antibodies. To prove this conclusion we can use some K negative red cells to adsorb the patient's serum or the patient's eluate, if we can remove all or part of the reactivity, then the guess is right. Sorry for my poor English, if it bring you some trouble to understand .

When we test a coagulate blood sample , we may get the positive C3d DAT result, this is not because the antigen and antibody reactive ,but because the blood coagulation is crosslinked with complement activation. In this question, I think all the positive result with screening cells and panel cells in RT with the same degree and neg in 37 degree C, we can get the conclusion that the antibodies is to a kind of high frequent antigen ,but not the autoantigen ,and the C3d DAT pos result can't give us the conclusion to autogentigen, too. Though lots of situation the conclusion is right,but I still think we need the autocontrol , it is necessary.

I don't think this conclusion is correct, because some disease can get the C3 DAT pos result ,such as DIC .

I think the heterozygous E and heterozygous c(R1R2) will be ideal. Because the fetus will not express homozygous E and c commonly,except some gene crossover or other gene change.

I am very interested in what is HTLA. Is it human T-lymphocyte antigens? And if it is why it will present on red cells? Thanks for any help.

Why not use auto serum add cells suspension be the negtive control instead of 6% Alb?

I think poly AHG can tell me the presence of complement dependent antibodies.

I had not encounter the IVIG cause HDFN, maybe it exist. I think to do the elution of the mother's DAT pos cells is a way to find the hemolysis reason.

I think the key is what is the relevant of DAT with the HDFN in ABO . We don't routinely do cord blood DAT if the mother is antibodies neg. And I don't think we need do DAT if the mom is neg and has no antibodies.

Sometimes pregnant can decrease the A and B expression of the RBCs. I think the reagent sensitivity is one reason and the pregnant is another.