danozol

has anyone treated with danozol

Yes, a few of us have. It can take a long time to work if it works at all. I was allergic to it (broke out in hives), so I wasn't on it very long.

stroder, I've been taking low dose Danazol since September of last year. It seems to work best for those with a strong (> 4 week) IVIG response. Has your doctor mentioned Danazol to you?

Sandi, I've been thinking about going to this years ITP conference, LOL. Go and do nothing but ask everyone about CRISPR as a possible eradication of EBV and thus ITP. Get others thinking about it. Sound like a plan?

Yep. Did it and had bad side effects. Didn't stay on it long. Hope it works for you, though.

Hal9000 wrote: Sandi, I've been thinking about going to this years ITP conference, LOL. Go and do nothing but ask everyone about CRISPR as a possible eradication of EBV and thus ITP. Get others thinking about it. Sound like a plan?

I'm trying to decide if this is sarcastic or not. As this is one of the areas my lab works on... At the emergence of ITP, CRISPR would be unable to solve anything. If EBV is playing a role in emergence of adult, chronic, ITP, then it's likely a recognition of an EBV protein, once you are producing anti-bodies, genetics isn't really playing a role anymore. I also wouldn't want to CRIPSR a living human, there's more off target affects than most people realize.

lurpelis wrote: I'm trying to decide if this is sarcastic or not. As this is one of the areas my lab works on... At the emergence of ITP, CRISPR would be unable to solve anything. If EBV is playing a role in emergence of adult, chronic, ITP, then it's likely a recognition of an EBV protein, once you are producing anti-bodies, genetics isn't really playing a role anymore. I also wouldn't want to CRIPSR a living human, there's more off target affects than most people realize.

lurpelis, take a look at this thread for the general idea. Most importantly, see the referenced page and video on CRISPR.
"Can CRISPR resolve many chronic diseases, like ITP ?"
pdsa.org/discussion-group/6-general-itp-discussion/30308-can-crispr-resolve-many-chronic-diseases-like-itp.html

Changing human genes is not the idea. Eradicating herpes viruses (eg EBV and Shingles) by leveraging CRISPR is.
Note that EBV hides in human B cells and high jacks many cell functions for it's own ends - and not for your immune system's benefit and function. Hence the reason it is thought to trigger so many different immune system diseases.
en.wikipedia.org/wiki/Herpesviridae#Human_herpesvirus_types

While leveraging CRISPR on humans seems like a potentially dangerous proposition, leveraging CRISPR on herpes viruses is likely much more benign and likely to become pervasive first.

You are working with CRISPR technology in some way?

I don't work with CRISPRs, but my colleague does and she's an expert in them. Generally speaking, our current thoughts on viral mediated autoimmune disease is that the virus is cleared long before the autoimmune disease presents itself. (Some data has show as long as 7 years prior.) This is more to do, again, with proteins in EBV (or some other virus) yielding anti-bodies that also recognize your own cells. There was a paper in the last two years discussing EBV proteins as the link between EBV and autoimmune diseases like type 1 diabetes and lupus.

lurpelis wrote: I don't work with CRISPRs, but my colleague does and she's an expert in them. Generally speaking, our current thoughts on viral mediated autoimmune disease is that the virus is cleared long before the autoimmune disease presents itself. (Some data has show as long as 7 years prior.)

From reports here, that sort of delay seems to be a common track for EBV and many cases of Chickenpox/Shingles viruses too. But I wonder about Influenza virus. That seems to be very quick. Just a few weeks at most.

How do your colleagues rationalize the long, up to multiyear, delay? Intuitively, EBV can only be cleared (on first exposure) after the immune system has taught itself how to destroy it. So a later recurrence flair should be dealt with quickly by existing T and B cell memory of its surface glycoproteins.

This is more to do, again, with proteins in EBV (or some other virus) yielding anti-bodies that also recognize your own cells.

Doesn't what I mention about EBV hampering B cell functionality (eg activation and division) potentially explain the long delays in the development of auto-immunity after first exposure?

There was a paper in the last two years discussing EBV proteins as the link between EBV and autoimmune diseases like type 1 diabetes and lupus.

Perhaps this is the article you were thinking of? Summary:
"Epstein-Barr virus and autoimmune diseases"
www.nih.gov/news-events/nih-research-matters/epstein-barr-virus-autoimmune-diseases
Abstract:
"Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity."
www.ncbi.nlm.nih.gov/pubmed/29662164

The second article is the one.

The delay is still not fully understood, but in IBD, there has been some evidence of long-lived plasma cells continuing to generate low levels of anti-EBV protein antibodies, which, over time, may simply degrade or change to spontaneously target self-cells.