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Bone Marrow Failure Causes, treatment approaches, terminology, related diseases |
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#1
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MDS, Aplastic Anemia, and Inflammation
I wanted to post this article that I found because, scattered throughout my posts on this thread, you will see that my son had Henoch–Schönlein purpura (a common childhood vasculitis) twice. A more serious course when 6 and a slight relapse when 7, then 6 months after the slight relapse he was diagnosed with Aplastic Anemia. Really, I believe he doesn't have "idiopathic" Aplastic Anemia, he has vasculitis affecting the blood flow into or out of his bone marrow, based on the several body wide symptoms that he had (least of which was that he couldn't control his body temperature. Unless he was on Prednisone it was either 97.5 or 99.5 degrees F - on Prednisone it was 98.6). Imagine a gas tank where you fill the tank with gas, but because of inflammation you pinch the gas line leading either into or out of the bone marrow. If the blood can't get in, or can't get out, the bone marrow can't do what it is supposed to do. We know from a series of tests that inflammation leads his numbers to go down. A series of searches led me to this.
http://link.springer.com/article/10....2247806#page-1 Henoch–Schönlein Purpura as Clinical Presentation of a Myelodysplastic Syndrome. I know, it's silly, I keep posting random things that I think will come together to form a cohesive "theory of bone marrow failure." Yet recently even the AAMDS facebook page posted a link between Myelodysplastic Syndromes, Autoimmune Diseases, & Inflammation: https://www.facebook.com/aamds "Moffitt Cancer Center Announces Development of Experimental Treatment for Myelodysplastic Syndromes, Autoimmune Diseases: http://www.marketwatch.com/story/mof...k=MW_news_stmp Well, hopefully this helps something. I would rather it be all in one place! |
#2
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Interesting post - I was diagnosed with MDS two years ago - but had hive like skin nodules, aches and fatigue for two years prior to the MDS diagnosis. Originally thought it might be Lyme Disease and was initially treated for that - but from whatever origin inflammation and autoimmune symptoms preceded any abnormal blood counts. I'm still not convinced the autoimmune process wasn't triggered by Lyme - or tick bites - that then triggered an autoimmune reaction in the bone marrow that turned into MDS...
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Lower risk MDS diagnosed 2012. Recurring skin nodules treated with prednisone, otherwise watch and wait. HG dropped from 11.5 to 8.7. Kept going down to 5. Vidaza didn't work. BMT from MUD on September 10 2015 |
#3
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Adding to your library
Another "random" article regarding immunity I read about yesterday. Has an interesting view on "naive WBC" versus those with memory, and how they impact aging, cancer and autoimmunity.
http://www.lef.org/Magazine/2015/1/H...-Aging/Page-01
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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. |
#4
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Something else to add: http://www.bloodjournal.org/content/124/25/3699
IFN-γ causes aplastic anemia by altering hematopoietic stem/progenitor cell composition and disrupting lineage differentiation Chronic intracellular infection can cause increased levels of IFN-gamma. Deb |
#5
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LLbrown,
I'm sorry I'm so late in responding. I've really been wondering about this: "Chronic intracellular infection can cause increased levels of IFN-gamma." If you think about it, it makes perfect sense. research has shown that cancer tumors are most often caused by a virus that the body's killer T-cells don't respond to, because you have too many regulatory T-cells. So in summary you have a chronic viral infection. In the case of autoimmune disease you have too many killer T-cells and not enough regulatory T-cells, so why not also from a viral infection? And in the case of Aplastic Anemia, why not a viral infection in your bone marrow or blood cells? You have the chronic infection either way (cancer or autoimmune disease), but there's something about your body that is trying to fight it off but can't. Marlene, Your article about exhausted T-cells is also very interesting. My son was 1 month premature and got RSV when he was 3 months old and fought it off wonderfully, actually, but I wonder if that primed his immune cells to prepare a massive attack for the rest of his life, and got tired from too many massive attacks, especially as we know his trigger is upper respiratory viruses. Additional Info: 1) I did finally find an article with a case of Henoch–Schönlein purpura (HSP) turning into Aplastic Anemia. http://link.springer.com/article/10.1007/s004310051239 It's from 1999. A 10-yr old boy developed 9 weeks' worth of Aplastic Anemia from Henoch-Schonlein purpura but they don't call it aplastic anemia, they call it pancytopenia, and it responded to erythropoietin (EPO). The boy eventually still needed a kidney transplant because he got the kidney damage that more often accompanies HSP, but luckily was ok after that. 2) Solaris (eculizumab), which is used to treat PNH, is in a phase two clinical trial at the University of Glasgow for treating Guillain-Barre Syndrome.: http://www.mctlawyers.com/new-treatm...arre-syndrome/ "The first new treatment for Guillain-Barre Syndrome in 20 years is entering a Phase II clinical trial. It’s called eculizumab, which is a humanized monoclonal antibody first approved by the Food and Drug Administration in 2007 to treat a rare blood disorder. In Guillain-Barre Syndrome, or GBS, the body’s immune system attacks part of the peripheral nervous system and often causes acute neuromuscular weakness. People with GBS may also experience numbness, tingling and blurred vision. Because this disease can affect respiratory muscles, some patients have be placed on a ventilator. Up to 30 percent of patients are left with a permanent disability, including some who cannot walk unassisted. ... Neurologists believe controlling inflammation during the acute phase of GBS is key to reducing nerve injury and long-term neurological problems. Eculizumab may help do that by inhibiting activation of the body’s complement system. This component of the immune system may become overactive in GBS and damage nerve fibers." |
#6
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Observing stem cells maturing into blood cells in living mouse
Date: February 12, 2015 http://www.sciencedaily.com/releases...0212131830.htm When Busch turned on the marker in adult animals, it became visible that at least one third (approximately 5000 cells) of a mouse's hematopoietic stem cells produce differentiated progenitor cells. "This was the first surprise," says Busch. "Until now, scientists had believed that in the normal state, very few stem cells -- only about ten -- are actively involved in blood formation." ... "When we transplanted our labeled blood stem cells from the bone marrow into other mice, only a few stem cells were active in the recipients, and many stem cells were lost," Rodewald explains. "Our new data therefore show that the findings obtained up until now using transplanted stem cells can surely not be reflective of normal hematopoiesis. On the contrary, transplantation is an exception [to the rule]. This shows how important it is that we actually follow hematopoiesis under normal conditions in a living organism." |
#7
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Wow me too.
Bingo thats me!!!!! No clue what triggered my pre blood inflammation hyper immune symptoms of MDS diagnosis but here we are. Im getting ready to try CBDs to see if they will heal my inflammation and see what happens from there.
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