I have news, friends and neighbors, very interesting news.
Though I don't have the actual report in hand, today I got the top line results from my recent bone marrow biopsy at NIH, courtesy of Dr. Bogdan Dumitriu.
The report on the marrow and aspirate (blood pulled from the marrow) were not all that newsy. I still have dysplasia (messed up blood production) in all three cell lines (reds, whites, and platelets). Blasts (immature white blood cells) are "around five percent." That's higher than they have been, but Dr. Dumitriu doesn't seem concerned.
I'll know more about all that when I get the full printed report from the Medical Legal Department at NIH.
But the big news was in the cytogenetic report, where we look for chromosomal abnormalities.
And the news was . . . normal. 46xy. No abnormalities. Bupkis.
What makes that remarkable is that previous BMBs have found abnormalities in as many as 16 of the 20 cells analyzed (80%).
Here's the track record:
Code:
Date Dup1q 8+ Normal
02/25/10 50% 0% 50%
03/23/10 40% 0% 60%
09/03/10 55% 55% 45%
10/19/10 55% 30% 45% (NIH)
05/17/11 80% 15% 20% (NIH Post-Campath)
08/12/11 40% 0% 60%
11/29/11 0% 0% 100%
From 80% of cells with messed up chromosomes to 0% in six months. What gives?
Here's the story I'm telling myself . . .
At some point, my marrow started churning out defective hematopoietic (blood producing) stem cells and progenitor cells. Some of those had broken copies of Chromosome 1. My immune system responded by developing a set of T-cells primed to attack those defective marrow cells. But the attack backfired, and the cells with the Chromosome 1 defect began to acquire another defect in Chromosome 8.
Last November, I received Campath at NIH. That knocked my T-cells flat, stopping the immune war in my marrow. It began to recover, showing improvement in my red cells, neutrophils, and platelets. Improving reticulocyte numbers showed I was making baby red blood cells. But then something stopped the improvement in my red cells: the too-short telomeres in my stem cells began making too many progenitor cells that just aren't viable; they die off before making red cells.
So the improvement in my counts stopped. But my marrow, despite the short telomeres, continued to heal. Relieved from the T-cell attack, the Chromosome 8 mutation subsided. Now the Chromosome 1 mutation is gone. I'm still not making enough red blood cells, but the threat that a mutant clone poses has lessened for now.
That's the story I'm telling myself, but what do the docs think?
Dr. Matt Olnes, formerly of NIH, told me "I think you are right on as far as your assessment of what may be happening with your marrow. I also think that the Danazol is a logical next step to improve your red cell transfusion requirements."
Dr. Bogdan Dumitriu, my doc on the Danazol trial, was a bit more reserved. It could simply be that the 20 cells cultured for the cytogenetic analysis happened to be normal. On the other hand, he suggested, the results certainly suggest that "things are stable (which is what we want) or even improving (cautious)."
Either way, that's my story, and I'm sticking to it. Now we just need the Danazol to kick in and give my poor stem cells a little more telomere to work with, so they can make more viable red blood cells and I need less frequent transfusions.