Real-world Insights into Crohn's, Ulcerative Colitis and other Gastro-Intestinal disorders.
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I'd like to let you know that Aussie Mediator is sponsored by OPC Health, an Australian supplier of prosthetics, orthotics, clinic equipment, compression garments, rehabilitation devices for doctors, physiotherapists, orthotists, podiatrists and hand therapists. If you'd like to know what OPC Health offers, visit opchealth.com.au and view their range online. Inflammatory bowel disease, or IBD, is a term that encompasses two major conditions, Crohn's disease and ulcerative colitis.

These chronic inflammatory disorders affect the gastrointestinal tract, causing symptoms such as abdominal pain, diarrhea, weight loss and fatigue. Beyond the gut, IBD can also lead to various extra-intestinal manifestations, adding another layer of complexity to its management. Inflammatory bowel disease is not just a physical challenge, it's a condition that deeply impacts patients' quality of life.

Understanding the causes, risk factors and treatment options is crucial for both medical professionals and patients alike. Today we'll explore the latest research and advances in treatment and the ongoing challenges of managing inflammatory bowel disease with insights from one of the experts in the field, Professor Jane Andrews, an expert in inflammatory bowel disease. Welcome to Aussie MedEd.

G'day and welcome to Aussie Med Ed, the Australian medical education podcast designed with a pragmatic approach to medical conditions by interviewing specialists in the medical field. I'm Gavin Diamond, an orthopaedic surgeon based in Adelaide and I'm broadcasting from Karnaland. I'd like to remind you that this podcast is available on all podcast players and is also available as a video version on YouTube.

I'd also like to remind you that if you enjoy this podcast, please subscribe or leave a review or give us a thumbs up as I really appreciate the support and it helps the channel grow. I'd like to start the podcast by acknowledging the traditional owners of the land on which this podcast is produced, the Kaurna people, and pay my respects to the elders both past, present and emerging. Today we're lucky enough to be joined by Professor Jane Andrews.

a specialist in managing inflammatory bowel disorders and other disorders of the gut. A gastroenterologist who's going to talk to us about inflammatory bowel disease, a group of conditions I used to get confused about when I was at medical school, not quite understanding between IBD and IBS, and perhaps she can explain in a bit more detail to me as an orthopaedic surgeon trying to get my head around it. I think it's a really good question, what's the difference really between inflammatory bowel disease and irritable bowel syndrome, because they've got very similar acronyms like IBD and IBS.

But the trick is in expanding out the name and thinking about the words because one is an inflammatory disease, so that's IBD, and the other one is irritable bowel syndrome. And so the bowel is irritable, it gives us lots of symptoms,

And it's defined syndromally by having a certain symptom pattern. So one has inflammation and tissue damage, and that's IBD. That's inflammatory bowel disease. And the other condition has a lot of symptoms but doesn't have obvious tissue damage. It seems to be more a brain-gut dysfunction. Right.

So if we start off with IBD then, or inflammatory bowel disease, I believe there's only two main areas of it, Crohn's and ulcerative colitis. Is that correct? Or are there other new subdivisions to it nowadays? Yeah, look, again, a really, really good question. And there probably are some subdivisions.

But there are two recognisable clinical entities and one is called Crohn's disease. And that's generally recognised because it is a full thickness inflammation of the bowel. So it goes through from the lining of the bowel, through the muscle coat and out to the cirrhosa.

And so it is associated with complications such as narrowing and perforation and fistula formation or tracks forming between the affected part of the bowel and other organs or other parts of the bowel.

Ulcerative colitis affects only the colon, so only the large bowel, and that's why it's called ulcerative colitis. You can get Crohn's colitis as well, but that is a full thickness inflammation, whereas UC affects predominantly the lining of the bowel, so the mucosal layer. And so it is generally...

less burden of disease unless it is severe. There are other little subtypes and genetically, when we've been involved in some studies with the International IBD Genetics Consortium, it has been noticed that

that ileal Crohn's disease genetically looks very different from both Crohn's colitis and ulcerative colitis. And they genetically look more similar. But when you see them in a patient, they look quite different.

And is the pathology different in itself apart from the areas which it affects? Yes, look, it is a little bit different. And there is a lesion which is regarded in medical terms as kind of like a signature of Crohn's disease, or we call it in fancy words, pathognomonic lesion.

And that is the formation of a non-caseating granuloma. Now, that's a very fancy way of saying that there are a lot of macrophages and what we call histiocytes, so a specific type of white blood cell that is accumulating in the tissue in the submucosal layers and looking like it's trying to fight an infection that it can't clear.

These granulomas were initially described in infections like TB in old-fashioned times, but they were what was called caseating granulomas because they formed casein-looking-like stuff or cheesy, pussy stuff in the middle. But the granulomas in Crohn's disease don't form the cheesy, pussy stuff, so they're called non-caseating granulomas.

only occur in about 40% of people with Crohn's disease though. So they're neither necessary nor sufficient to make that diagnosis. It's more taking the whole picture together. It's not a diagnosis only on pathology. You have to take the clinical scenario, the endoscopic picture, the radiological picture and the histology together really.

And with ulcerative colitis, you said it's actually a predominantly mucosal layer that occurs in the colitis. And what sort of pathology do you get in that? You don't get the granulomas and it depends on the severity of the disease. But with the mild disease, what you see is some really superficial erythema or redness and swelling. And then what you see is infiltration of the mucosa by chronic inflammatory cells. So if there's only acute inflammation, we

With only neutrophils, that doesn't make a diagnosis of IBD because for either Crohn's or UC, you have to have chronic inflammation. So you have to have some macrophages and lymphocytes. And you have to have some chronic changes of tissue damage. So with UC, you will get crypt branching and you will get shortening of the crypts in the lining of the bowel. So you get a more simplified mucosal epithelium.

So the ulcers that you get in ulcerative colitis, they look much different to the sort of aphthous ulcers that all of us get in our mouths on occasions and things, or does it look very different? Yeah, it does look quite different. The aphthous ulcers that you mentioned that we get in our mouths, so those little sort of white lesions, they're actually the earliest lesion in Crohn's disease, aphthous ulcers.

And, you know, you see them in a patchy fashion when the disease, you know, if you catch it very, very early. And it just looks like a whole crop of little mouth ulcer sorts of things. And they can be in the colon or in the ileum.

In ulcerative colitis, the first lesion seems to be really some swelling and redness in the bowel. So when we do an endoscope, what we see is that there is a loss of the normal mucosal pattern. So we can't see the blood vessels underlying.

and it's friable, which means that if you touch it or you put too much air in, it tends to bleed spontaneously, and then it can get deeper ulcers. And in ulcerative colitis, the changes tend to start at the rectum,

and expand up continuously for variable distance around the colon. Whereas in Crohn's, it tends to be, whatever you're seeing, it tends to be patchy. So they present symptomatically in different ways or can they look very similar? Yeah, so it's most dependent on the site of disease as to how they present.

So whether it's Crohn's colitis or ulcerative colitis, people who have inflammation of the large bowel present in the same way.

And they will present in the same way that people of lots of other forms of colitis get as well. They will have pain, increased stool frequency, urgency and blood in the stools. So colitis presents as a very typical syndrome of an irritated, inflamed, bleeding colon. So you'll have all of those features. And the different thing with Crohn's is that it commonly affects the ileum.

So even if the colon is involved as well,

the ileum will be involved in about 70% of cases. And people with ileal involvement will commonly get obstructive symptoms. So 20 to 40 minutes after eating, they may get right iliac fossa pain, bloating, distension, and they may have diarrhea as well. They may even have tenderness. And if they're slim and they lie down, they might find that they've got a bit of fullness if they feel their right iliac fossa.

Right, so two different ways of presenting in some ways. Obviously, there are other causes of colitis too, such as like an infection that you get with a gastro. Does that look like a colitis or they look completely different in that sort of way as well? Yeah, look, it's a really good question because the main differential for the first presentation of colitis, if it's an inflammatory bowel disease type of colitis, the main differential is always infection. And that's because infection happens much more commonly.

And even in someone with known Crohn's colitis or ulcerative colitis, infection has to be ruled out every time. Because just because you've got IBD doesn't mean you can't get gastroenteritis. Patients travel, they get Shigella, they get Salmonella, they get amoebiasis. So infection is really, really important. And if people are immunosuppressed...

and they have IBD, we have to also think about unusual causes of colitis like CMV and Clostridium difficile if you've had antibiotics. So infection is a big thing to rule out both on a first presentation and on any flare presentation.

What other differentials would you think of that she'll mimic or can look like either of these conditions? So if someone's just got a lot of diarrhoea and abdominal pain, irritable bowel syndrome or IBS is our other really big diagnostic problem. That's actually quite easy these days because if someone's got symptoms that's going for more than about six weeks, so we know infection's not the problem,

Then if they don't have obvious blood in their stools and they look otherwise well, we recommend that the GP does a test called the fecal calprotectin. And that is measuring a stable protein that is found in white blood cells. And so if the calpro level is up in your stools, it means that you have inflammation in the bowel or mucosal disturbance.

And that's enough to say it's not IBS, it might be something else. So the younger group, IBS, is the big differential for everybody, infection. And then in the older group of people, ischemic colitis is the one we don't want to miss. I'd like to let you know that Aussie Med Ed is supported by HealthShare. HealthShare is a digital health company that provides solutions for patients, GPs and specialists across Australia.

Two of HealthShare's products are Better Consult, a pre-consultation questionnaire that allows GPs to know a patient's agenda before the consult begins, as well as HealthShare's Specialist Referrals Directory, a specialist in Adelaide Health Directory helping GPs find the right specialist.

Okay, and that obviously presents in a sudden fashion a deteriorating patient. Yes, and typically ischemic colitis will present with pain first and blood and diarrhoea later, whereas with IBD typically there will be sort of a trickling up of diarrhoea and pain is a very late feature and blood will often come before pain.

And ischemic colitis just relate more to atherosclerosis of the branches of the descending aorta. What about thromboembolic episodes as well? You know, obviously you can get thromboembolic episodes. They don't tend to be as common to the gut and I think it's

because of the anatomy and the twists in the vessels they tend to go predominantly you know as cerebrovascular accidents to the brain the ischemic episodes we get in the gut tend to be in people with really quite bad vascular disease a lot of vascular calcification when you do their ct scan you might think they've already had contrast but they haven't there's so much calcium there

What sort of patients get inflammatory bowel disease? I've read somewhere that in Crohn's particularly it's often in the younger person under age of 30. So the peak age of onset is between about 29 and 39 years of age. However, 10% of people with IBD are diagnosed under 18 and people diagnosed under 18 tend to

tend to have more severe disease, although when we've done transition studies, they do tend to settle down as they reach adulthood and they tend to have pretty reasonable outcomes over time.

Interestingly, we looked some years ago when I was a registrar in New South Wales, and we found that consistent with the older literature, there is a bimodal distribution, particularly for Crohn's. There's another peak in the older people. I guess I shouldn't say older now because I think it starts kicking up at around 60 and going through to 70 something. So we do have quite

a number of older people with IBD and that's because the incidence is going up in the community overall and also our young people with IBD don't die early so if you're diagnosed early you will be an older person with IBD at some stage so the incidence and the prevalence are quite different.

Right. You've implied a couple of things there. First of all, the increase in incidence is really interesting. And also the other factor too that you mentioned in talking about that is the fact that they don't die. Obviously in the past this was something that was quite serious and led to morbidity. What's the reason why people are living longer with Crohn's disease? Yeah.

Look, I think it's probably multifactorial. We're all living longer in our Western developed nations than we were when I graduated from medicine. People in general are living longer and also we do have better treatments. So certainly for ulcerative colitis, people used to die of acute severe colitis until Sydney True Love published on the use of steroids for rescue therapy. And I think that was only in the late 50s or early 60s. And we really only got

Other really effective therapies when we got the advent of the monoclonal antibodies, and the first one to come into the market was infliximab, and I think the first published study was in 1984. We didn't get access on the PBS till 2007 in Australia, but that really did revolutionise people with ulcerative colitis care because they no longer lost their colons on their first episode of acute severe colitis, and we were able to then...

you know, get them through that and get them onto other maintenance therapy.

We learnt a lot about how to use cheap old drugs. Azathioprine was a mainstay of maintenance therapy for many years. I guess we're moving a little bit away from that as people get older because there are cumulative risks when you've been on the drug for many years of lymphoma and skin cancers and the risks go up with age and also with male gender. So we're a little bit unkeen for the over 65 men to be using thiopurine therapy.

We do have a lot more other drugs, mostly reasonably pricey. However, if we only look at the cost of the drug and not look at the benefit to the community in terms of being able to work, being able to stay in role, not being in hospital, not having a stoma, not using a lot of appliances, then

then I think the cost-benefit equation comes out really very favourably. So, you know, life expectancy is normal for almost everybody with IBD. So it's really quality of life that's important. Now, we've talked also about the fact that it's going up and increasing in incidence as well, and I believe there's a genetic element to it. But what actually is the cause of this? Is it purely an autoimmune disorder triggered by some factor we don't know, or is there more to it than that?

Look, I think that's the $6 billion question or $6 gillion question. Clearly, our genetics have not changed in my lifetime. And medically, the incident's gone up hugely. We're set to hit about 1% to 1.5% of the Australian population being affected by 2030, which is only six years away. So it's not a genetic change.

The genetics have to be permissive, if you like, but it is a polygenic disease. And even with the risk scores that have been developed, having a higher risk score doesn't guarantee you're going to get it. And having a low risk score doesn't guarantee you won't get it. So we were very excited about 15, 20 years ago with the Human Genome Project and the IBD International Genetics Consortium.

However, we've come to realise that we really need to look more broadly at the environment, particularly what we call now the exposome, which is what you're exposed to, which goes into your gut, which will influence what is in your internal environment. And it's food, it's microbes, it's other chemicals, it's viruses, it's the fungome.

And really, it's a fancy way of saying we don't understand this. However, we do know that if you eat fresh fruit and vegetables and you're exposed to a sort of a not too clean environment when you're younger, so you have a vegetable garden, you have a pet in the family, you play outdoors, your risk of getting either UC or Crohn's is lower than average. We know that if you're breastfed, your risk is lower. Right.

And we know that in adulthood, if you have high fat content in your diet, you have lots of sugars, you're in a higher risk group. So I think while we don't know the precise cause, we do know a lot of things that are lifestyle-based that we can do to reduce risk. Truly amazing, because we've done a recent interview regarding Parkinson's disease and talked about the microbiome being a significant factor in the cause of Parkinson's.

So it's turning out that the gut really is a major risk for a lot of conditions. And so this is another one. Yeah, I think that's true. And like I was going to be a little bit flippant and say I became a gastroenterologist because, you know, the gut's at the centre of the universe. However, I think the important thing to be aware of is

is that the gut is really a bit like the skin. It is a barrier between the outside and the inside. However, unlike the skin, the gut is really rich in its exposure to a whole lot of messenger substances. And they sit there for a long time in very immediate and direct contact with us.

We know there's a lot of mucosal immune crosstalk between the contents in the gut and the internal contents of our body. And we know that germ-free animals who don't have that education of their immune system have higher rates of many diseases. And we know that there are specific pathogens that are involved in triggering some things. So, you know, I think that what we're finding is

is not surprising in a way when we think more broadly that, you know, it's not just a black box anymore. We've got this whole messenger system exposed to our internal barrier. And so is it purely an autoimmune response that triggers this actual pathology or is it actually an attack of an unknown substance? Look, we don't know. I don't think we know exactly.

If it were something very specific though, and it was only one substance, I actually think we probably would have found out a little bit more now with the really large analytical techniques that have been applied. I suspect that the problem is that it is a combination of factors that belong to the individual and

to their environment, and then to their choices. So what you eat, where the food was grown that you had, how much detergent you use, things that happened in your childhood. And it's not to blame parents because we know parents have a lot of guilt about feeling that something was a childhood environment.

I guess the best we can do, though, is to try and adopt a public health approach to ensure that we have really good education to help people minimise habits and practices and

that make many of these autoimmune-type diseases more likely. So sterilising your kitchen and only eating things that have been nuked in the microwave is probably not best practice for your gut. In Crohn's and ulcerative colitis, I believe you can also get other areas affected. I've seen it in the rheumatological conditions, but also I believe you can get skin disorders as well and eye conditions as well. What are the other main conditions that need to be considered when talking about Crohn's and ulcerative colitis as well?

Yeah, so they're really important things and sometimes they can occur before the diagnosis of inflammatory bowel disease. So we call them extraintestinal manifestations and the typical ones is someone presenting with a sore red eye, so an iritis. You can also get episcleritis, but iritis where vision is affected is what we worry about. And then, of course, mouth ulcers can be an initial thing that people get troublesome and recurrent crops of aphthous ulceration.

Then on the skin, there are a couple of pretty typical conditions that really often they're pathognomonic. So they're often absolutely barn door. Oh, my goodness, we need to look at your gut. And one of them is pyoderma gangrenosum. And that is a really nasty, punched out ulcer that can look quite deep and it's got violaceous edges. And it really photo is usually enough to

And it's terrible, though, because occasionally someone will biopsy one of those ulcers and then it just makes it all worse. So if you ever think that you see pyoderma and it's a punched out nasty ulcer, please don't biopsy it. Please take a photo because that's often enough.

And then the other skin condition is called erythema nodosum. And that as well is really quite obvious. I had a patient one day who was traveling and she was in Alice Springs and she rang me and she said, can I send you a photo on email?

I think I've got erythema nodosum. So she'd looked at her legs and she'd gone on to Google and she'd diagnosed it herself. And they are lumps that are exquisitely tender. Again, they're kind of reddy, brawny, violaceous kind of appearance.

and absolutely exquisitely tender, and they're typically down the front of the shin, then there are all the joint conditions. So they can be associated with typical spondyloarthropathies, where you get the sacroiliac joints and the spine and

oligoarticular large joints involved. And that's the typical sort of arthritis, but you can also get some small joint problems. People used to be taught in the old textbooks that these things would cycle either in or out of sync with the inflammatory bowel disease. That was before we actually got a lot of access to colonoscopy though and good quality CT scans.

We used to just judge whether the IBD was active on symptoms. What we found when we looked a bit more closely was that almost all of these other inflammatory extraintestinal manifestations cycled into activity when your gut was active.

And are those things like the erythema nodosum, are they pathognomonic as well or are they just things that are associations that can occur? Oh, no, they're pretty pathognomonic. I mean, my understanding, it's pretty rare to get them without gut inflammation. Apart from the actual clinical manifestations, what other ways are assessing them? You mentioned in passing the colonoscopies and CT scans.

What's your order of actually further investigating someone who you're thinking has got an inflammatory bowel disease? Yeah, look, I think that's a very good question. So it does come back to what we think the differential diagnosis is. So if it's a young person and they've got grumbling symptoms but there's no obvious blood and they look well, then in that scenario, a faecal calprotectin and a simple full blood count or CBE, whatever you call it,

are really good first tests because if someone doesn't have iron deficiency and you can see that on the CBE right because you look at their red cell indices you don't need iron studies up front but if the MCB or the MCH is low and even if the hemoglobin is normal then you can be suspicious also the platelet count will often go up if people are either iron deficient or they've got inflammation and also the white cell count might go up too so you get a lot of information off a simple blood count

And the calprotectin is a really good test because if the blood count and the calpro are low and normal and the person doesn't have overt rectal bleeding, weight loss, night sweats, tender abdomen, you can be really happy that a person under 50 has got IBS and we don't need to do further tests. They can move on then to treatment with a low FODMAP diet or symptom management or stress reduction, all sorts of approaches.

If someone, though, does have an abnormal CBE and they've got an elevated calprotectin, then probably that's a time to get your iron studies done, get chemical pathology to look at the albumin and the liver function tests. And if you're not a gastroenterologist, that's a really good point at which to call your local gastroenterologist.

Because if someone's got iron deficiency and they don't have another good reason for it, and they've got an elevated Calpro, then someone needs to think about what's going on in their gut. And then it will depend what our access to intestinal ultrasound is like.

and whether we think there's ileal disease, whether we go with ultrasound or MR enterography first, or whether we go with the colonoscopy first. So that's probably a judgment call for us as a gastroenterologist, because I think

You know, the order in which we do things will depend a little bit on the scenario before us. And what would make you decide which test you'd choose to use first in that scenario? Is colonoscopy the main treatment or main diagnosis? Yeah, it's the commonest one, particularly if someone's got colitis symptoms or they've got overt rectal bleeding.

Absolutely. And if you do think that it is Crohn's disease, you need to get into the ileum. And the reason we would do the colonoscopy predominantly as the first next test after thinking that IBD was likely is so that we could get tissue.

because we really want to make sure that we can look at it and that we can get tissue to rule out other things, you know, like CMV or clostridium difficile or cancer, you know, particularly if you're looking at the older person. So I think that we need to make sure what we're dealing with before we go and get on to some drug therapy. Okay. And we

When you have made the diagnosis, I believe some monitoring or regular surveillance is required by regular colonoscopies or possible endoscopies as well. And what's the sort of plan in that situation? What is the basic treatment once you've made the diagnosis as well? Yeah, look, the basic treatment depends a little bit whether it's Crohn's or UC and the disease location and severity.

I guess, suffice to say, we have some treatments that are really good for induction of remission, so getting people into remission, and some of those then go on to be used as maintenance treatments, but sometimes we use a different maintenance treatment. However, what we're aiming for is to get someone into remission and then to keep them there.

And so we have some tests that we will do to see, have you hit remission yet? And they will be tailored to what drug we're using, because if we are using a drug where we expect it's going to take, you know, three to six months, then we're not going to look before the three to six month mark. We might use the fecal calprotectin test to see that it's coming down. And if someone had an elevated CRP, we might also use that to see that it's coming down. And

Probably you wouldn't want to be doing it more often than six to 12 weekly, unless you had a very sick patient where you may be admitting them to hospital to stabilise them. That is actually quite rare these days, needing to admit people, because we're pretty good with remote monitoring. Now, in terms of when you do a next colonoscopy,

That will depend a little bit. So if someone with ulcerative colitis goes reasonably quickly into a good remission and their calprotectin goes back to the normal range and their bowels go back to just normal, formed stool, no urgency, no blood, then probably around the one year mark, you want to do a scope to make sure they have hit remission, verify that they're in remission, and then they can just be monitored with symptoms and Calpro once a year.

We don't need to do cancer surveillance kind of colonoscopy until someone has had disease for eight years or more, or unless they've got a high-risk problem like PSC, primary sclerosing cholangitis, which really inflates the cancer risk. And those people have an annual colonoscopy. Right. And for Crohn's disease, do you do endoscopies and colonoscopies? Yeah. So it's interesting that because the paediatricians do an endoscopy on everybody, right?

We rarely find much of interest on the endoscopy, so we don't do an endoscopy as standard for people with Crohn's disease in adult care. If someone has symptoms, we will do an upper endoscopy, but again, it's mainly colonoscopy. If they have colonic Crohn's disease that affects more than one third of the colon, then they have to go into a surveillance program for colorectal cancer, just the same as the people with ulcerative colitis.

So we divide the colon into a scoring system of six pieces. So the rectum, sigmoid, descending colon, transverse, ascending colon, cecum. And if you've got more than a third of it involved, then you follow the same rules of once you've had eight years of disease or if you have PSC, that you have regular surveillance colons. While we're on the topic, how far down can you get with an endoscopy and how far up can you get with a colonoscopy?

Well, it does depend a little bit on how determined you are and what the need is, right? Because we don't just go as far as we can for the hell of it to show how clever we are with a scope. It's really tailoring your endoscopic exam to what you need to do and what you need to find.

So if you're using a standard upper GI endoscope, you should be able to get into the third part of the duodenum pretty regularly. And how far that is in will depend on the height of the person, because the esophagus is one of the main lengths. And if you're a six foot five guy, you've got a much longer esophagus than a five foot two kind of person. So it's probably

Probably somewhere in the order of 70 to 100 centimetres from the top end. We do have single balloon and double balloon enteroscopy available and we also have push enteroscopy. So if someone really needs to get further down the small bowel, we have other techniques available.

We only use them rarely. And they're usually in older people to treat bleeding lesions so that they don't need to go and have a laparotomy and meet our upper GI surgeons. They're not usually needed for IBD patients. And for colonoscopy, we should almost always get into the ileum. We should be able to go up the ileum somewhere between 5 to 20 centimetres.

It's rare to need to or to be able to get up more than that with the standard colonoscope. And that's, again, to do with the length of scope that's required and also the complexity of the number of corners one has to navigate. Again, you can use a double balloon and you can go up further and

there's got to be a compelling need to do that. Okay. Well, let's go on to the treatment. We haven't actually really touched too much on the treatment yet. So we've got a diagnosis. We're trying to get them into remission. Perhaps go through the Crohn's and ulcerative colitis and how the treatments vary. Yeah. So it's kind of a whole lecture on its own, I think, but we divide things into simple old-fashioned cheap things and more

expensive advanced therapies. So simple old-fashioned cheap things. A lot of people with ulcerative colitis who present in the primary care and ambulatory care, secondary care setting, they can be managed without steroids and many of them just need

oral 5-ASA or mesalazine preparations and they are not really absorbed. They deliver into the colon and they dissolve and they act like a cream that self-applies itself to the lining of the bowel and

And the main thing there is to use doses that are high enough. And if someone's got a flare, you should use topical therapy by enema, rectum, suppository or foam. Because if you use what we call top and tail therapy, which is oral and topical 5-ASA, people go into remission faster.

And you can use either oral or topical therapy in 5-ASAs for maintenance. If someone's only got proctitis, then a suppository three times a week can be great.

Some people don't like suppositories, then they need to take oral therapy. But if you've got extensive disease affecting more than just the rectum, you probably need an oral 5-ASA. Steroids are kind of something that we use from time to time, less and less these days because they rot your bones, they give you diabetes, they make you fat, they give you acne, they disturb your sleep, and they make you at higher risk of infection if you use them longer term.

But they are a get-out-of-jail-free card, and if someone really needs settling down quickly, a short burst of oral steroids is acceptable.

But we say that you should never use them unless you know what you're going to use next. So if you're needing to use steroids, you need another strategy because that means that the person was not well. Sometimes you need to admit people for IV steroids. And if they don't respond really well within three days, they should start on a biologic for rescue. And usually we would use infliximab. Although nowadays we've got some new drugs which are oral called JAK inhibitors and

And there is an emerging experience on using JAK inhibitors for acute severe disease, but that's early days. Maintenance therapy for UC, 5-ASAs or mesalazine, the maintenance therapy workhorse. Some people then need to go to an immunosuppressant, and they're usually in the thiopurine class of drugs, so MS.

azathioprine, 6-MP, thiaguanine. For Crohn's, they are used a lot. They do, though, develop a cumulative risk over many years for skin cancers and lymphoma. So after about the 5 to 10-year mark, we are now feeling increasingly uncomfortable and looking to move people on to other therapies.

And that's where we've got a lot of newer drugs. So we've got anti-TNF antibodies. We've got anti-IL-1223s. Ustekinumab is in that group. We've got drugs which prevent lymphocyte trafficking into the mucosa. And we've got azanamide, vedalizumab, and atrazomide all in that group. And vedalizumab has been around for a long time, but azanamide and atrazomide are orals that we're just developing experience with.

And look, there's a lot coming up in the marketplace as well. So the thing there which is good is there are a lot of options and we still try and use each one well because if you're going to have disease for 40 or 50 years, we don't want to waste a therapy by not using it well. This makes me think while you're speaking about all the different therapeutic agents.

How many would have been around when we first started medical school and now how many there are now and how big the expansive area of medicine is over those years and what will happen in the next few years as well. Exactly. We're learning a lot more immunology. I think the basic principles of treating IBD, though, remain the same. Try and be logical. Try and make sure you understand what is the problem for that patient today and also what are the risks and benefits of doing something or nothing.

Because doing nothing is an active choice as well. I'm a firm believer in proactive care. And if there is a problem, step in, assess the problem and make some decisions. Don't let things drift. So proactive care is really important. Now, are those agents the same ones you'd use for Crohn's as well? They generally work both conditions, yeah. You mentioned surgery then. So sometimes surgery is required. Is that often or is that occasional? Surgery.

Surgery is often something which has been presented in the past as a last resort and not a good idea. I've always worked hand in glove, literally sometimes, you know, with the colorectal surgeons because when they need us, they really need us. And when we need them, we really need them. And actually, if you're the patient, you really need to know that your surgeon and your physician are friends and that they trust each other.

Because that is absolutely vital, that communication. And today we've had our usual every two weeks MDT. We had one colorectal surgeon online. We had another two in the room. We had all the trainees. We had five gastroenterologists, the IBD nurses, the psychologists, the dietician, medical students,

We had pathology in the room. We had radiology in the room. And then we did clinic. And then we had clinic wrap up. And it's a team-based sport because there are a lot of things that these patients need us to consider and get right. And none of us can be across every bit of it.

So Jane, what are the main surgical type procedures they might undertake? What are the things that we might just need to be aware of? So for ulcerative colitis, if you come to need surgery, you generally need a colectomy. And that's because it affects most of the colon and you can't really leave bits of it behind.

particularly if you're having a colectomy because of dysplasia or cancer or cancer risk, we must remove the whole colon. And then there's a choice as to whether people have a stoma long-term or whether they get a restorative proctocolectomy where the surgeon will fashion what's called a pouch and sew that down low onto the anal verge.

And we have a number of people with long-term pouches. We also have a number of people who are quite happy with their stomas. So when you see the rate of having a colectomy is proportional to how many years you've had colitis for, and it goes up every decade. It is lower than it used to be, though. Many more people are keeping their colons because we don't lose them on the first severe episode because we've got better rescue therapy. And also, we're not having as much chronic grumbling disease that's

that turns a lovely floppy colon, which is a nice storage organ,

into a hosepipe. Because if you get that chronic inflammation and everything just jets through your colon, even if it's not inflamed, you have diarrhea and incontinence. So colectomy actually can make your life a lot better. So if you've got incontinence and long-term diarrhea, colectomy can actually make your life amazingly good. And people need to know that. It can be a good thing. What's the chance of someone who develops ulcerative colitis needing a colectomy?

Look, the old data are probably not the same as the new experience. So if we look at the older data, though, about 30% at 30 years of disease duration, I don't think we're going to be seeing that now because it's already flattening out the curve. So, you know, that's really good. I saw some very nice data the other day on the rate of intestinal failure from Crohn's disease.

And that has really dropped. I mean, that's gone from being a significant risk for people to being in the last kind of

going down to a vanishingly small percentage. So that's excellent news. And the typical surgery in Crohn's disease is to remove the narrowed area of the ileum because the ileum is a narrow area of the gut. And if it gets scarred, it can become a stricture or a blockage. And so taking out that narrowed area and rejoining the bowel so there's no stoma involved, that's a really common operation in Crohn's disease.

And that really gives people a great result. And in the past, it used to be just an operation and off you go. Whereas now it's an operation and we use medications to make sure it doesn't come back. And we're not doing it again in five years and then again in another five years.

If we just have the last few minutes of time, and this is probably going to open a can of worms, because I looked at inflammatory bowel disease, and obviously it's inflammation against an unknown substance or an unknown condition causing autoimmune disorder. As opposed to celiac disease, we get inflammation from a known substance. Yes. How are the conditions, apart from knowing what was causing it, how...

How does it look different, either Crohn's or ulcerative colitis versus celiac disease? Really good question. Part of the clue is, you know, because we're very simple people, we gastroenterologists, perhaps even more simple than the orthopedic surgeons. But, you know, it's nowhere near the colon. It's up in the duodenum. So the first thing is that it's a proximal GI disorder and it affects the duodenum from the proximal extent and goes distally with increasing severity. It actually...

can look a little bit like ulcerative colitis endoscopically,

in that it simplifies the mucosa. So it makes the mucosa look flat and less detailed. However, when you look at it microscopically, it doesn't look like ulcerative colitis. It's got very particular infiltration with what are called intraepithelial lymphocytes. And so you have to count the number of that. Well, we don't count them. The pathologist counts them for us. And you also get the long villi, which are very, very long and finger-like in the duodenum. They become very blunted and you can actually get them really flat.

And the thing with that that's important is that you turn something in the small bowel, which is the mucosal surface area, it's actually as big as a tennis court, our small bowel surface area, to absorb things.

And once you go from having the nice long villi to having the really flat things, what you do is you turn the tennis court into, you know, kind of like a quarter of a cricket pitch. And so clearly your ability to absorb nutrients really drops off and it affects the proximally absorbed nutrients first. So iron and folate. And so people become iron deficient and folate deficient and they lose weight. They calorie waste. Yeah. So it's quite different. And

Although, you know, the ligand, which is in gluten, although it triggers a very specific immune response, it's kind of not autoimmune in a typical sense because there is a trigger that when you remove the trigger, that disorder really settles down in most people. So it's really just a matter of removing gluten from the diet and being obsessive about it and that fixes the condition. Yep.

There are some treatments coming, though, where we are experimenting with creating immune tolerance for people with celiac disease so that they then can consume gluten. And we actually were involved through the Royal Adelaide Hospital Gastro Service and CMAX in a couple of phase one studies looking at developing immune tolerance. So watch this space because it's common. A lot of people are looking at whether they can modify that response.

And then there's that grey zone of irritable bowel syndrome and gluten intolerance. Oh, yes. And that almost seems to go hand in hand together. And is that a mild form of celiacs? What causes it? It's just the actual amount of stock hitting the bowel that actually just flares up the irritable bowel syndrome. Yeah. Look, it's a commonly confused area.

So there is not really any condition that we can define biochemically that is gluten intolerance. You either actually have celiac disease or you don't. What people are describing, though, is they're describing that they imperfectly absorb all the components of gluten in their diet. And high gluten diets tend to be high in other things that are encompassed in the acronym FODMAP.

So you may have heard and a lot of people have heard of the FODMAP diet. It's not the FODMAP diet because that would mean you would get worse. It's the low FODMAP diet, actually. It's removing FODMAPs from your diet. But it's talking about fructans and other oligosaccharides and cellulose and artificial sweeteners. There's a whole group of things which we don't perfectly all absorb. And some people have a lower absorptive capacity for them than other people.

And so what happens is that these things which are imperfectly absorbed go through to your colon where they get fermented.

And people with IBS have a lower threshold for perceiving fermentation, i.e. distention, as being unpleasant. And they also tend to get more diarrhea. So it's a very interesting area because you can have people who don't absorb these things and who get diarrhea, but don't get pain, don't get disturbed, don't go to a doctor. So by definition, they don't get a diagnosis of IBS.

But I always remember this one young male patient of mine came along with these terrible, very typical IBS symptoms. And they'd only come on about eight, nine months before, which was a little bit unusual. Often people have had the symptoms for a long time. So I had a chat with him about what had changed in his lifestyle because he was clearly very healthy otherwise. Well, he'd moved in with his new girlfriend.

And he couldn't fart in front of her. So the whole thing, because he couldn't pass wind, meant that he was getting this terrible abdominal pain. But he was working as a roofer during the day and he was letting the wind go free and he was very comfortable. As soon as he got in his car, picked up his girlfriend to go home...

Terrible pain, terrible problems. So, you know, the thing with IBS is it's really interesting. Sometimes the problem is social rather than medical, and it's very important to tease that out with the patient because it's not a condition where it's necessary for you to change your diet. It's not a condition where it's necessary for you to have a drug to prevent tissue damage. The treatments are all for your comfort. Right.

Well, it's been fantastic hearing all these different conditions and learning more about it, particularly learning that it's actually healthy to fart as well. Yes, and it's really good for you to eat the fart foods because they reduce your risk of bowel cancer. So all the brassica vegetables and pearl barley, very, very good for you. Well, luckily we're in a different studio so I can see you comfortably. It's been fantastic speaking to you, Professor Jane Andrews. Really appreciate your time and thank you very much for coming on Aussie Media. Thank you for being here. You're very welcome.

Thank you very much for listening to our podcast today. I'd like to remind you that the information provided is just general advice and may vary depending on the region in which you are practicing or being treated. If you have any concerns or questions about what we've discussed, you should seek advice from your general practitioner. I'd like to thank you very much for listening to our podcast and please subscribe to the podcast for the next episode. Until then, please stay safe. I'd like to let you know that Aussie Mediated is sponsored by Avant Medical Legal Indemnity Insurance.

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