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Interesting research/articles/videos etc.

Hello everyone,

I was recently diagnosed with Crohn's disease affecting my terminal ileum (for now). Fortunately, I was very asymptomatic because I experienced a few days of abdominal discomfort and thereafter went on with my life without severe symptoms. I could eat anything and do anything. However, some of my blood markers were a little contradictory and my GP pressed for an endoscopy. Better safe than sorry, I went on and they found smaller than 1mm aphthous spots in my TI. The mental blow was harder than the physical one I must admit. Started with Budesonide and doing the same as before haha. Before taking the first dose, my blood was tested again and my CRP was 0.5 therefore I am very interest in how they will 'measure' the effectiveness.

Coming to the point of this thread. I am very optimistic and interested in recent research and found already nice stuff on this forum regarding medical breakthroughs and research. I am planning to post some things I find myself on the internet here and hopefully some nice discussion about it will unfold. Besides, I hope other people will contribute with interesting stuff they come across on the internet.

Yours sincerely,

K
 
To start,

I just saw this video with some nice information:


Very short summary:

It outlines some current treatments and new treatments in the near and far future. The speaker nicely compares several drugs for their efficiency etc.
 
Also, I did some further digging on the video of Mark Sundrud (posted in another topic, so wont do that again). Here is an overview of some publications:

https://sundrudlab.com/papers/

Especially the most recent publication is interesting in my perspective:

Bile acids are lipid-emulsifying metabolites synthesized in hepatocytes and maintained in vivo through enterohepatic circulation between the liver and small intestine1. As detergents, bile acids can cause toxicity and inflammation in enterohepatic tissues2. Nuclear receptors maintain bile acid homeostasis in hepatocytes and enterocytes3, but it is unclear how mucosal immune cells tolerate high concentrations of bile acids in the small intestine lamina propria (siLP). CD4+ T effector (Teff) cells upregulate expression of the xenobiotic transporter MDR1 (encoded by Abcb1a) in the siLP to prevent bile acid toxicity and suppress Crohn’s disease-like small bowel inflammation4. Here we identify the nuclear xenobiotic receptor CAR (encoded by Nr1i3) as a regulator of MDR1 expression in T cells that can safeguard against bile acid toxicity and inflammation in the mouse small intestine. Activation of CAR induced large-scale transcriptional reprogramming in Teff cells that infiltrated the siLP, but not the colon. CAR induced the expression of not only detoxifying enzymes and transporters in siLP Teff cells, as in hepatocytes, but also the key anti-inflammatory cytokine IL-10. Accordingly, CAR deficiency in T cells exacerbated bile acid-driven ileitis in T cell-reconstituted Rag1−/− or Rag2−/− mice, whereas pharmacological activation of CAR suppressed it. These data suggest that CAR acts locally in T cells that infiltrate the small intestine to detoxify bile acids and resolve inflammation. Activation of this program offers an unexpected strategy to treat small bowel Crohn’s disease and defines lymphocyte sub-specialization in the small intestine.

I hope that a company does further invest in this possible pathway. It may not be THE holy grail but as Sundrud explains in the video, it is a possible cause in a portion of patients. Elaborating on that, after reading quite some publications I think that a lot is trashed in the Crohn's disease corner while it is possibly not one but several different diseases and just suppress the immune system. But I think things are changing as some people mentioned earlier on this forum.
 
Lastly (for tonight),

I saw that Takeda mentions the Sibofimloc/ Fimh blocker in their pipeline on the website and it is planned for FY2025 for now. Anyway, very interested in the read-out of the phase 2 trial in early 2023!

Have nice evening.
 
I really didnt like that S.Hanauer latest video, a future of combo biologic immune supression. Don't like the sound of that.

In my eyes he is positive about taking treatment completely further in the wrong direction. We want safer more targeted drugs, not double immune supression that is very non targeted.

But welcome Kilicad, great to have another person here interested in the research side of things.
 
Thank you westernbuddy! I agree that the immune suppression approach with biologicals is something we hopefully won't need anymore in the coming 10 years or so. But I think there are some promising drugs currently being researched such as Sibofimloc.
Anyway I found this slightly outdated overview on a website with new treatments in advanced stages:

https://www.frontiersin.org/files/A...-651415-HTML/image_m/fphar-12-651415-t001.jpg

And also this market analyses:

https://www.emjreviews.com/gastroen...disease-cells-surgery-and-novel-therapeutics/

I am very interested in the new kids on the block, the JAK inhibitors. There are some contradictory signals but hopefully they will become a new treatment approach for all those people who fail(ed) other treatments. Long term remission rates etc is something I am very interested in. Worrying is the risico profile of some with reactivation of Herpes Zoster and the lack of endoscopic remission in filgotinib.

In that light, the Risankizumab trial show some very promising results with endoscopic remission. As an Il-23 inhibitor, thus similar to Ustekunimab, it is exciting to see the endoscopic remission rates of 39% and 29% in deep remission for moderate to severe crohn's disease patients!

More info about this: https://news.abbvie.com/news/press-...sponse-and-clinical-remission-at-one-year.htm

I was also looking for videos of the lates (A)IBD conference in the U.S. but could not find them right away, if someone does have links or material please let me know, thank you in advance!

Have a nice day.
 
Also, people on Twitter and interested in news or views on Crohn's disease treatment, I would recommend to follow the people behind 'Propel a Cure for Crohn's disease' This is their website:

https://www.propelacure.org/

They are also the ones with the videos in the other posts with Mark Sundrud and Brian Coombes. Anyway some of the founders are on Twitter and show some interesting insights / threads about treatments etc.

Also the twitter of the IBD conference with some interesting pics, therefore if someone has the videos, I am very interested!

https://twitter.com/IBDConference
 
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Today I discovered this interesting research (link below). I did read the previous research of them (I think from 2009) and it gives valuable insight in the (changing) clinical course of Crohn's disease in a population based study in Norway. This new study published only the collected data but I suspect that interesting insights will follow.

The 2021 research:
https://www.tandfonline.com/doi/full/10.1080/00365521.2021.1922746

Anyway, it does not give many insights right now but interesting to follow!

The 2009 research with insights is also interesting but notice that the biological era just started and this a big factor is in disease course:
https://www.cghjournal.org/article/S1542-3565(07)00888-9/fulltext

Conclusion of the 2009 study:
"The prognosis for CD seems better than previously reported. The probability of surgery was low, and fewer than expected developed complicated disease behavior. Nevertheless, the cumulative relapse rate of 90% and the finding of prognostic risk factors for subsequent surgery might call for attention to early effective medical treatment strategies."

Very exciting to see a new analysis with the recent data!
 
Sibofimloc
Sibofimloc, which is currently the only drug candidate targeting the underlying cause of the disease, is in a Phase 2 trial in post-operative Crohn's disease and a data readout is expected in H1 2023.
 
Hello Crohn2357 and artheta,

I did read the SSI website (Q biologics) but I think they are rather quiet for some time, citing that further research depends on funding. Hopefully more on that in future.

Regarding the MAP vaccine and rhb-104, I thought the trials of rhb-104 were a bit disappointing. I am aware that it has similar remission rates as some biologicals but for a drug that was claimed to be the 'solution' for Crohn's disease, at least in theory by some, was not what I expected. Anyway, it could still be possible that MAP is the cause for some patients, and this may be the cure but I don't think it will be the solution for every patient. Still hoping that the vaccine trials will prove me wrong haha.

Stem cell therapy was something with exciting developments especially for fistulas.
 
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https://www.hindawi.com/journals/ijr/2013/610393/

Anyone some opinion on this research? It is quite old but and it is not often cited. Nevertheless, the publication mentions trials with Rifaximin to treat Crohn's disease and the mentioned remission rates are pretty impressive. I've found a current phase 2 trial with Rifaximin, looking forward to the results.
 
https://www.hindawi.com/journals/ijr/2013/610393/

Anyone some opinion on this research? It is quite old but and it is not often cited. Nevertheless, the publication mentions trials with Rifaximin to treat Crohn's disease and the mentioned remission rates are pretty impressive. I've found a current phase 2 trial with Rifaximin, looking forward to the results.
I did a course of rifaximin without any lasting effect, though of course, only one data point isn't significant by itself
 
Location
San Diego
https://www.hindawi.com/journals/ijr/2013/610393/

Anyone some opinion on this research? It is quite old but and it is not often cited. Nevertheless, the publication mentions trials with Rifaximin to treat Crohn's disease and the mentioned remission rates are pretty impressive. I've found a current phase 2 trial with Rifaximin, looking forward to the results.
It's not often cited for a good reason. I don't know anything about that particular paper, but I do know that the publisher, Hindawi, has a poor reputation and has been accused of freely publishing low-quality results.

Over the past 15 years or so, the once conservative and respectable business of scientific publishing has been invaded and polluted by dozens, even hundreds, of so-called "predatory journals" that freely publish all kinds of nonsense that range from the merely low-quality to the outright fraudulent. The hallmarks of a predatory journal is that they are usually open access (although there are a few legit open access journals), they are frequently published out of Asia or the Middle East, and their so-called "peer reviewers" are people unknown in the scientific discipline and are sometimes merely friends and family of the predatory publisher.

And according to some observers Hindawi fits the description. They may not be outright fraudulent, but I tend to look at the stuff Hindawi publishes with a dubious attitude.

Experienced scientists usually don't have much trouble separating the wheat from the chaff among scientific publishers, but sometimes young scientists just starting out make the mistake of publishing their work in one of the questionable journals. And the unsuspecting general public is usually completely fooled by these journals.

If you want to read more about this phenomenon, google "predatory journals."
 
It's not often cited for a good reason. I don't know anything about that particular paper, but I do know that the publisher, Hindawi, has a poor reputation and has been accused of freely publishing low-quality results.

Over the past 15 years or so, the once conservative and respectable business of scientific publishing has been invaded and polluted by dozens, even hundreds, of so-called "predatory journals" that freely publish all kinds of nonsense that range from the merely low-quality to the outright fraudulent. The hallmarks of a predatory journal is that they are usually open access (although there are a few legit open access journals), they are frequently published out of Asia or the Middle East, and their so-called "peer reviewers" are people unknown in the scientific discipline and are sometimes merely friends and family of the predatory publisher.

And according to some observers Hindawi fits the description. They may not be outright fraudulent, but I tend to look at the stuff Hindawi publishes with a dubious attitude.

Experienced scientists usually don't have much trouble separating the wheat from the chaff among scientific publishers, but sometimes young scientists just starting out make the mistake of publishing their work in one of the questionable journals. And the unsuspecting general public is usually completely fooled by these journals.

If you want to read more about this phenomenon, google "predatory journals."
here is an article you might find interesting, its from 2012.
link
 
It's not often cited for a good reason. I don't know anything about that particular paper, but I do know that the publisher, Hindawi, has a poor reputation and has been accused of freely publishing low-quality results.

Over the past 15 years or so, the once conservative and respectable business of scientific publishing has been invaded and polluted by dozens, even hundreds, of so-called "predatory journals" that freely publish all kinds of nonsense that range from the merely low-quality to the outright fraudulent. The hallmarks of a predatory journal is that they are usually open access (although there are a few legit open access journals), they are frequently published out of Asia or the Middle East, and their so-called "peer reviewers" are people unknown in the scientific discipline and are sometimes merely friends and family of the predatory publisher.

And according to some observers Hindawi fits the description. They may not be outright fraudulent, but I tend to look at the stuff Hindawi publishes with a dubious attitude.

Experienced scientists usually don't have much trouble separating the wheat from the chaff among scientific publishers, but sometimes young scientists just starting out make the mistake of publishing their work in one of the questionable journals. And the unsuspecting general public is usually completely fooled by these journals.

If you want to read more about this phenomenon, google "predatory journals."
Hello Scipio,

I already thought it to be a little shady when coming across other research from this specific journal. Thank you for the explanation! I will keep an eye on this in the future. Last thing I want is to spread disinformation or something similar.
 
Interesting to read! hopefully this will lead to some very specific and targeted drugs. Still far away but somewhere I am hopeful that one day Crohn's disease will be something that isn't life altering anymore and it can be effectively treated.

Have a nice evening.
 
Hello everyone,

Here an article about EEN in adults and how it works (mechanism).

https://www.dovepress.com/exclusive...iew-of-cli-peer-reviewed-fulltext-article-CEG
From the article:
The per-protocol subgroup analysis showed a difference in remission rates for both adults (RR 0.82, 95% CI 0.70–0.95) and children (RR 1.43, 95% CI 1.03–1.97).
This seems to be saying that an adult being on EEN is even less likely to achieve remission than an adult who isn't on it. I can't really explain that, other than that I may be misinterpreting it.

But for children, EEN does appear to work. Maybe this has something to do with the longer disease duration in adults, and progression to stricturing or fistulizing Crohn's.
 
I have read in the past it's not as effective the second time.

I have experienced that, 1st time doing ENN as an adult, felt like my crohns had been hit with an Army, deep remission very fast.

2nd time ten years later, no where near as effective, and I don't know why exactly, just putting out the inflamation it was not as effective.
 
I think this is one of the better articles I've read so far. It perfectly explains some things I already mentioned between the lines on this site:

Schermafbeelding 2022-01-18 om 21.53.12.png

Especially these lines about the figure above: "Each patient is exposed to and lives in a particular corner of the world, creating a distinct exposome, the genome is determined at the time of conception, and the gut microbiome results from a myriad of dietary and other factors that start right after birth and act for the rest of one’s life. Consequently, when an IBD factor initiates the chain of events that will eventually result in IBD, each patient will use different receptors, activate different signalling molecules, bind different DNA loci, express and transcribe different genes, translate different proteins, and produce distinct pro-inflammatory products. These products may differ, but all will induce a damaging inflammatory process that will be recognised as IBD at the clinical level (Figure 1)."

Simply put, it is just too easy to just look at Crohn's disease as one simple disease where A causes B. It is something we (especially in the Western world) think too often: thinking in singular causations. But maybe just look at it like a complex network of different nodes interacting and creating the symptoms we experience. This does not exclude the possibility that a certain factor does affect all people with the several versions of Crohn's disease.

Anyway, the last part of the article is really something that needs to be explored. Nowadays there is so much information, so many data entries. I really think that Crohn's disease patients are a group with the richest database in the medical world. Just think, how often do people need to draw blood, measure their Cal-P, do genetic test etc. All these datapoints need to be scraped together and analyzed, on a large scale, say continent size preferably. This simple step, can give us the insights in the different way people go through their disease and which tiggers are predictors. The article about a link between Epstein-Barr Virus and MS, published a few days ago, is a perfect example about how this can be done (https://www.science.org/doi/10.1126/science.abj8222).

In conclusion, nice article and a really fresh look at where we are. But who is gonna act?

Have a nice evening!
 
I have read in the past it's not as effective the second time.

I have experienced that, 1st time doing ENN as an adult, felt like my crohns had been hit with an Army, deep remission very fast.

2nd time ten years later, no where near as effective, and I don't know why exactly, just putting out the inflamation it was not as effective.
i recall reading about the effects of een on the microbiome and there was some evidence that it reduced diversity in the microbiome, this could be a good thing and a bad thing depending on which microbes were affected, i vaguely recall a more detailed study that did show some good microbe were less diverse after een, and why this might be is that it is a low fiber regimen, which may encourage the loss of good bacteria. So this could be one reason why it loses its effectiveness as it could be partially damaging, but so is bowel prep/lavage for colonoscopy so, either way, its all making it worse in the long run just like antibiotics are doing. Microbiome research will make a great positive impact on medicine that's for sure, but it will take time to refine these new studies, before its all applied to the current medical system.
 
please look at the date. Not so very recent although it may not be too relevant as to date since it's just an analysis of increasing incidents of Crohn's in one country. Maybe it means better diagnosis, more well trained doctors, more patient awareness. Who knows.
Hi Crohn’s dad,

I noticed that it was from 2014. Nevertheless, this message was referring to a link I posted in the post before (and a similar study but older). Maybe I should've referred to that particular post. Anyway, my bad. About the relevance of the study; I think it is interesting to compare the studies of different time periods and see if the course of the disease is changing. This will tell more about effectiveness of certain new drugs etc. For example, in the next decade we will hopefully see the surgery rate coming down for Crohn's disease. I've read multiple articles claiming that it is significantly declining but a comprehensive study is missing. To add, in the next several years a lot of new drugs will hit the market which will also alter the surgery rate (hopefully).

In a way this thread is just a nice diary for myself and post some interesting links that others might like too. In the future I hope to look back at these and think: "we've come a long way since then ;)"

Have a nice evening.
 
 
Based on it's specificity, we should expect guselkumab to behave like and be a competitor to Stelara.
Yes but also developed by Janssen so I guess it is profitable enough for them to add another biologic. I know it is not a definite solution but yet it is another option for patients who fail other drugs. There is just a lot coming in the next years.
 
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Location
San Diego
Yes but also developed by Janssen so I guess it is profitable enough for them to add another biologic. I now it is not a definite solution but yet it is another option for patients who fail other drugs. There is just a lot coming in the next years.
Yes, and mirikizumab (Eli Lilly) is another IL-23 specific antibody that is working its way through the clinical trials to market. The success of Stelara in IBD has not gone unnoticed.
 
Still reading and re-reading some of the interesting research presented and posten during ECCO22

The data regarding Guselkumab is in my eyes quite a game changer; 73% in clinical remission at week 48 (patients with modere to severe Crohn's!). That's quite something which I didn't encounter so far in other studies. Still it has the same MOA as Risankizumab/SKYRIZI (not sure though) which has lower results. Still, very promising results, yet it is a phase 2 study so still a year or three until it hits the market I guess?

Schermafbeelding 2022-02-22 om 22.23.55.png

Also look at the percentages of Ustekinumab in comparison, which had the same research set-up (same developer). Really interesting to see future studies. I also think it is a good signal that this already get's a big podium for a research in phase 2.

Link to article:
https://www.ecco-ibd.eu/publication...analyses-from-the-phase-2-galaxi-1-study.html
 
Guselkumab sounds really promising. Note that it's already approved for psoriasis and could be prescribed off-label for some patients. Same goes for Risankizumab.
 
Location
San Diego
The success of Stelara has been noticed by the drug companies, so they are all pursuing anti-IL23 drugs. Ustekinumab (Stelara) binds the P40 subunit and thus blocks both IL23 and IL12. Newer drugs guselkumab, risankizumab, tildrakizumab, and mirikizumab all bind the P19 subunit and thus block only IL23 - which is believed to be the key one for controlling Crohn's. They are all in various stages of development as IBD treatments and most have already been approved for psoriasis.

It's not clear to me why any of them would work better than Stelara, since Stelara also blocks the IL23. If that observation holds up I suppose it can be attributed to some technical difference between the drugs.
 
Hi all,

Just posting a personal update. I've been on Budesonide since December and doing well. Had a Fcal test and it was <5 and my blood was also good several times. Question now is, what to do after the Budesonide? My GI is leaving the choice up to me (bad decision hahaha). The choice is: doing nothing (no meds) or aza/6-mp. I've been reading a lot and I know that Crohn can mess you up in the long term so I'm leaning towards taking the meds but on the other side there is that little voice that says that maybe not taking meds is also an option. I've small bowel Crohn's disease.

My values:
first flare
CRP:50
Fcal : <15 ( still not buying this one haha but maybe because of small bowel?)

Doing fine:
Fcal: 210 (haha could not believe it)

Before starting budesonide:
CRP: 0.5

During Budesonide:
CRP: 0.5
FCal: <5

What are your thoughts? Appreciate all answers.
 
Location
San Diego
This looks very experimental at this point. The drug in question is a monclonal antibody that binds CD3 - a protein on the surface of cells in the thymus and in T-cell white blood cells. Apparently when it binds it decreases the secretion of cytokines (proteins that stimulate the immune response). So this drug acts at an earlier stage in the immune response than say Remicade or Stelara. Instead of directly blocking the cytokine as they do, it prevents the white blood cell from producing the cytokine in the first place.
 
This looks very experimental at this point. The drug in question is a monclonal antibody that binds CD3 - a protein on the surface of cells in the thymus and in T-cell white blood cells. Apparently when it binds it decreases the secretion of cytokines (proteins that stimulate the immune response). So this drug acts at an earlier stage in the immune response than say Remicade or Stelara. Instead of directly blocking the cytokine as they do, it prevents the white blood cell from producing the cytokine in the first place.
Does this mean that it's more on the preventive side than on the treatment side?

We need hope, Scipio... hope. :/
 
Location
San Diego
Does this mean that it's more on the preventive side than on the treatment side?

We need hope, Scipio... hope. :/
More of a treatment. Suppressing the immune system is a serious business. I can't imagine that any medicine that suppresses the immune system would get FDA approved for treating healthy people (to prevent a disease they don't yet have). The target population would need to be suffering from a significant illness of some sort in order for the benefits of immune suppression to outweigh the risks.
 
More of a treatment. Suppressing the immune system is a serious business. I can't imagine that any medicine that suppresses the immune system would get FDA approved for treating healthy people (to prevent a disease they don't yet have). The target population would need to be suffering from a significant illness of some sort in order for the benefits of immune suppression to outweigh the risks.
Got it. I was thinking if a person's "marked" for IBD (maybe later on when we are able to identify the disease via genetics) then this type of proactive treatment will outweigh the risks?
 

my little penguin

Moderator
Staff member
@asadmom
Even identical twins who have the same genetics only have a 33% chance if developing crohns if the other twin has it .
Same with siblings -33% chance
A lot of folks have the genes but don’t develop the disease .
 
Hi all,

Just posting a personal update. I've been on Budesonide since December and doing well. Had a Fcal test and it was <5 and my blood was also good several times. Question now is, what to do after the Budesonide? My GI is leaving the choice up to me (bad decision hahaha). The choice is: doing nothing (no meds) or aza/6-mp. I've been reading a lot and I know that Crohn can mess you up in the long term so I'm leaning towards taking the meds but on the other side there is that little voice that says that maybe not taking meds is also an option. I've small bowel Crohn's disease.

My values:
first flare
CRP:50
Fcal : <15 ( still not buying this one haha but maybe because of small bowel?)

Doing fine:
Fcal: 210 (haha could not believe it)

Before starting budesonide:
CRP: 0.5

During Budesonide:
CRP: 0.5
FCal: <5

What are your thoughts? Appreciate all answers.
Update:

GI insisted to not take any meds, because I was doing so well and my lab values were that good. I tried to explain that I had no problems taking meds but she said to wait and see. So it has been a couple of weeks now without budesonide and everything is fine. Still asking myself why did I take budesonide at all because my levels were fine before I started.

Next step would be azathioprine.
 
Hello everyone,

Little update on my personal situation. Doing very well, eating and drinking what I want and going on with my life. Now 1.5 month without any meds I decided to check my Fcalpro. And I'm very pleased with the result: again <5.

In short, I am very grateful and thankful for this and my current situation. However, this disease always makes you doubt. With limited ileitis it is not always that obvious to measure your disease activity with Fcalpro and sometimes I have some very small issues with fatty food resulting in flatulence. Nevertheless, I can deal with it and do not feel bothered with it during my daily activities.

Hoping that everyone has a nice day and I am sure that one day it will get better for everyone.
 
Our doctor is not a fan of it. Interestingly enough, many experts in the field are not too pleased with its safety profile.
I agree that the safety profile is of concern but nevertheless the choice of drugs is increasing with a lot of options coming. I think that in the next two years we'll have the choice of something like this:

1) Infliximab/Adalimumab/Cetrolizumab (anti-TNF)
2) Vedolizumab (Integrin)
3) Ustekinumab (il-12/23)
4) Risankizumab/Mirikizumab/Guselkumab etc. (il-23, there are slight differences between them -> will look up)
5) Upadicitinib/Filgotinib (Jak-1/3)
6) Etrasimod/Ozanimod (S1P)
7) Azathioprine/6MP etc. (IMM)

The point is, there will be a lot to use before ending up with a surgery and it will decrease surgery rates and debilitating disease for most. Nevertheless, my critique (like everyone else) is: they are all focussing on the immune system with the concerns of adverse events like infections. Hopefully promising new pathways to treat Crohn's disease will emerge.

Since my diagnosis I've tried to read a lot about new treatments and one of the things I think is really interesting is the effectiveness of EEN and there are new trials with (solid) food looking to mimic this effectiveness. Funnier is that they still don't know how and why EEN works.

Another important discussion going on now is the re-classification of the disease and in my opinion one of uttermost importance. I think that a lot of different diseases affecting the GI tract are al labelled Crohn's disease and this limits the research looking for treatments and causes. For example: take one of the phase 3 trials of one of the drugs mentioned above. How is it possible to measure effectiveness in proven different diseases (e.g. colonic crohn's / ileal crohn's / ileocolonic crohn's / VEO-ibd). I would really like to see a table with results where they divide those phenotypes because it is just unfair to throw them together. I think we should be going towards a clear divide in these diseases because they are NOT ONE disease. Furthermore, even persons with only ileal disease may have a different disease. In sum, this whole umbrella term called 'Crohn's disease' is just halting progress and you just can't find one perfect cause or treatment when you're examining 20 different diseases just because it is in the GI-tract and not UC. (end of rant haha)

Have a nice evening!
 
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