special antigen typing

Hi,
Hope you are all doing well.I am not sure this is the right place to post my question. When my son was about to be transfused the first time I asked for extended phenotyoing and genotyping like you advised. I think they did only the phenotyping. Anyway b/c of this his blood bag always has a sticker listing special antigen typing. Up until now it was always C, K and E neg. Last time however the sticker was complicated. E and K are still  neg. but C pos . Additionally it says JK9-pos and e( with a line on top ) pos and then another e ( with a line on top) neg.
I asked the doctor and he just said it doesnt matter since he hasnt had a reaction before. He said this is the closest match they have at the time.Can anyone explain this to me? I am sort of worried b/c he is already pale at less than two weeks instead of the usual 4. He hasnt been sick but did get a hep A vaccine.
Zahra

Sorry Zahra, I have got no idea about that stuff, but i should salute you for taking care of this matter. It is far more easy to try to avoid antibodies than dealing with them. I guess you can still do the genotyping test as it deals with the patients own genes. Please anybody can correct me if i am wrong

manal

http://www.merck.com/mmpe/print/sec11/ch146/ch146e.html

Delayed hemolytic transfusion reaction

Occasionally, a patient who has been sensitized to an RBC antigen has very low antibody levels and negative pretransfusion tests. After transfusion with RBCs bearing this antigen, a primary or anamnestic response may result (usually in 1 to 4 wk) and cause a delayed hemolytic transfusion reaction. Delayed hemolytic transfusion reaction usually does not manifest as dramatically as AHTR. Patients may be asymptomatic or have a slight fever. Rarely, severe symptoms occur. Usually, only destruction of the transfused RBCs (with the antigen) occurs, resulting in a falling Hct and a slight rise in LDH and bilirubin. Because delayed hemolytic transfusion reaction is usually mild and self-limited, it is often unidentified, and the clinical clue may be an unexplained drop in Hb to the pretransfusion level occurring 1 to 2 wk posttransfusion. Severe reactions are treated similarly to acute reactions.

With the amount of transfusions that thalassemics receive, it is almost inevitable that there will be occasional antibody reactions that do cause the red blood cells to be destroyed more quickly, resulting in a shorter interval between transfusions during the period that this reaction is taking place. If antibody problems persist and an increase in frequency of transfusion is the result, the first line of treatment is usually prednisone.

The phenotype of the blood that is used for matching before transfusions, includes all antigens native to the patient, along with all new antigens that are introduced through transfusions. The genotype is only which antigens the patient originally had, and this can be determined with a test of one's DNA. Genotype matching will produce a closer match than phenotype matching, but genotype blood matching is not widely available. This is a situation that will not change quickly either, because simply finding enough blood for the demand is a major task, and finding blood that matches the genotype can become very difficult, without a sufficient blood supply in general.