Qu Biologics Announces Initial Results in Crohn’s Disease Clinical Trial

Successful and moving forward


http://www.qubiologics.com/qu-biologics-announces-initial-results-in-randomized-placebo-controlled-crohns-disease-clinical-trial/?platform=hootsuite

Wow, this looks really interesting. Thanks for sharing, I wanna keep an eye out for this one!

Check this part out, found it on their Ulcerative Colitis page:

"Both patients had full resolution of symptoms and were able to discontinue all medications including SSI treatment. One of the patients was in remission for 17 months before having a recurrence, and the other patient remains in ongoing clinical remission (since October 2012) without any medication."
http://www.qubiologics.com/clinical-trials/ulcerative-colitis/

Now this looks like "case study" results--it's only 2 patients and not placebo controlled or blind by any means--but interesting that they took the patients off of the medication and were able to have sustained remission. Does this mean the goal of this medication is to induce remission, and then reduce/eliminate medication?!

Thanks for posting Jonny. I know a lot of people were wondering when this one would come out. Myself included.

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It seems to be falling in line with the specific MAP/Ecoli T-cell response study, where people with Crohn's disease have separate lines of T-cells responding to both MAP and Ecoli. The difference being that those with Crohn's are responding to MAP far more often than Ecoli. The study is called 'Increased frequency of intestinal CD4+ T cells reactive with mycobacteria in patients with Crohn’s disease' -2013 not the 2009 Version.

The interesting point in this study is that people with Crohn's Disease have reactive T-cells to MAP in the same range as those with Celiac Disease have reactive T-cells to Gluten - or transglutaminaze2 really.

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Anyway - It' looks like it might help at least a small subset of patients that are having a reaction to E-coli. It will also be interesting to see what happens and how many will achieve remission or lasting remission at the end.

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EDIT: The T-cell study also suggests some with UC might actually benefit from SSI Treatments as a small subset has active T-cell response to E-coli bacteria.

Post Edited (Canada Mark) : 3/21/2016 5:24:13 PM (GMT-6)

Canada Mark said...
Thanks for posting Jonny. I know a lot of people were wondering when this one would come out. Myself included.

-----

It seems to be falling in line with the specific MAP/Ecoli T-cell response study, where people with Crohn's disease have separate lines of T-cells responding to both MAP and Ecoli. The difference being that those with Crohn's are responding to MAP far more often than Ecoli. The study is called 'Increased frequency of intestinal CD4+ T cells reactive with mycobacteria in patients with Crohn’s disease' -2013 not the 2009 Version.

The interesting point in this study is that people with Crohn's Disease have reactive T-cells to MAP in the same range as those with Celiac Disease have reactive T-cells to Gluten - or transglutaminaze2 really.

----

Anyway - It' looks like it might help at least a small subset of patients that are having a reaction to E-coli. It will also be interesting to see what happens and how many will achieve remission or lasting remission at the end.

-----

EDIT: The T-cell study also suggests some with UC might actually benefit from SSI Treatments as a small subset has active T-cell response to E-coli bacteria.

SSI is essentially killed bacteria that is derived from E-coli and injected into the body so you 'trick' your body into thinking it has an infection so you get all of the benefits of acute infection (ie it stimulates the body's innate immune system to reverse the underlying chronic inflammation) with none of the negatives

Its explained in this video. https://www.youtube.com/watch?v=T4PpOj-dzR8

jonny_Murray said...
SSI is essentially killed bacteria that is derived from E-coli and injected into the body so you 'trick' your body into thinking it has an infection so you get all of the benefits of acute infection (ie it stimulates the body's innate immune system to reverse the underlying chronic inflammation) with none of the negatives.

Just as only relatively recently we learned, to everyone's surprise, that ulcers are caused by bad bacteria treated by antibiotics, there seems to be more and more research indicating that IBD may be a bacterial infection (MAP?) as opposed to an autoimmune disease. Already there are some people here who get relief from symptoms after taking a course of antibiotics.

I wonder if eventually we will learn that doctors who now treat IBD by suppressing the immune system, as opposed to strengthening the immune system, will turn out to be on the wrong side of history.

MAP still isn't widely found in uc patients.

The infectious disease hypothesis is interesting but far from proven to be true. Uc could still very well be an autoimmune disorder. I feel it's far to early to rule that possibility out.

Uc shows increased immune involvement and responds to immunosuppressive drugs, cause or symptom? Having gut bacteria out of wack, cause or symptom? All unknowns.

I'm just glad that the scope of what they're studying is increasing, and lots of possibilities are being researched. Maybe one of the hypothesises might prove to be true, or at least inspire new thoughts and hypothesis that ultimately are right.

Right, let's keep this discussion rational. Nobody has said that MAP infection is definitely the cause of IBD. Only that there is more and more reason to look at infection as being a possible cause of IBD, or at least CD. Every couple of weeks there is at least one thread pointing in that general direction:

https://www.healingwell.com/community/default.aspx?f=38&m=3595710

the article said...
New research commissioned by the UK government has also revealed evidence that MAP may be the cause of Crohn’s.
In the report issued a few months ago by the Government’s Advisory Committee on Dangerous Pathogens, Dr Ingrid Olsen said: “Together with all the genetic susceptibility emerging over the last decade, it is very hard to reject the hypothesis of mycobacteria being involved in the development of CD.”