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Very interesting. I don't think they went back to check John's telomere lengths once they understood the role they play in this disease. Finding the gene could be very helpful in determining the course of treatment I would imagine.
There have been a few with VSAA and SAA who failed AGT and were later found to have shortened telomeres.
I'm sure there are many unanswered questions surrounding this. Do those with the gene mutation all end up with blood disorders or does it need to be activated by some environmental trigger before it causes disease.
It would be good if they could go back and check everyone who has been diagnosed prior to this discovery.
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Marlene, wife to John DX w/SAA April 2002, Stable partial remission; Treated with High Dose Cytoxan, Johns Hopkins, June 2002. Final phlebotomy 11/2016. As of July 2021 HGB 12.0, WBC 4.70/ANC 3.85, Plts 110K.
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