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Tony,
This is very interesting. My son has SAA with a 19% PNH clone. He had ATG in July and is on Cyclosporine, we are waiting to see if it works. I have always had in the back of my head that his SAA may be B rather than T cell related. I.e. rather than his T cells being the problem that his T cells are reacting to a problem being caused by his B cells. The reason I say this is that two years ago my son had a common childhood B cell autoimmune response to some unnammed virus, he had Henoch–Schönlein purpura (HSP). He got the purpura and the swelling that goes along with it, but recovered from it fine in less than a month with no lasting complications. Then last summer he had a very sight relapse - had a few spots on his legs but not the swelling or arthritis. Recovered nicely in a couple of days. Then he got sick in April (looking back probably started in March) with a nasty upper respiratory virus (he tested positive for Rhino-virus or enterovirus, the test didn't distinguish which it was) and came down with Aplastic Anemia. He began to recover on his own in May but then went downhill again, and when he did his viral symptoms from April came back. My suspicion is that his body has a B-cell overreaction to viruses. We went to three hospitals for consultations and each hematologist I talked to doesn't know of a connection between the two (HSP or AA) or why that would happen. Of course HSP is much more common than AA. I actually asked once why different auto-immune diseases caused by many of the same factors are treated with different drugs, e.g. Rituximab, Intravenous immunoglobulin (IVIG), etc. I would have liked to have tried Rituximab. At the same time I realize that our doctors are hematologists, not immunonogists, and luckily all of the doctors I've talked to are very good at treating AA patients, and really my son needed to be treated ASAP. But I probably need to talk to an immunologist at a large university, mainly for my own curiosity at this point since we already did the ATG.
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