Jose Scher, MD

Hello, and thank you for joining this MEDcast series titled “

Concurrent Management of Inflammatory Bowel Disease and Psoriatic Arthritis

.” I am Dr David Hudesman, co-director at the Inflammatory Bowel Disease Center at NYU Langone Health in New York.

I’m Dr Jordan Axelrad, director of Clinical and Translational Research at the Inflammatory Bowel Disease Center at NYU Langone Health in New York.

In this program we’ll discuss strategies for managing coexisting inflammatory bowel disease [IBD] and psoriatic arthritis, and the importance of a multidisciplinary approach to providing comprehensive care. To discuss more of this, we are joined by Dr Jose Scher, Steere-Abramson Associate Professor of medicine and rheumatology at the NYU Grossman School of Medicine, New York. Thank you so much for joining us. Let’s begin.

Jordan, just to kick off this discussion, talk about extraintestinal manifestations [EIMs] in inflammatory bowel disease? How often are we seeing this? What are the most common types?

Sure. Extraintestinal manifestations are disease findings that are external to the GI [gastrointestinal] tract in patients with inflammatory bowel disease. In some studies, these are incredibly common. Up to 40% or 50% of patients may have an extraintestinal manifestation of their IBD, inflammatory bowel disease. These commonly involve skin, joints, liver, kidney, eyes, really any organ outside of the GI tract. Skin and joints tend to be the most common, which hopefully we’re going to get into today, but these can be incredibly difficult to manage and may require expert consultation with colleagues in rheumatology or dermatology.

We’re happy to have our expert here, Jose. Jose, on the flip side, in your rheumatology clinic, how often are you seeing GI symptoms or something that concerns you that there might be something underlying, some type of subclinical bowel inflammation or IBD in your rheumatology patients, specifically psoriasis and psoriatic arthritis?

Thank you both for the invitation. It’s a pleasure to be here. I’d say it’s fairly common if you take the entire spectrum of manifestation. By that I mean, in general, we would see somewhere in the order of 5% of our patients with psoriatic disease and/or axial spondyloarthritis having clinically overt IBD or concomitant IBD. The intriguing part of it is that depending on the studies up to half of our patients have a form of subclinical, meaning not clinically evident gut inflammation, which may or may not manifest itself over time.

I think such high rates on both ends of the spectrum that the collaboration is extremely important. For us, we see some of that data as well, as Jordan was alluding to, especially when we’re looking at arthralgias and spondyloarthropathies, rates as low as 10% to upwards of 50%. So when you’re seeing a patient like that in your office, what’s the usual workflow when you’re concerned about any subclinical GI inflammation? Are you sending anything into your office? Are you referring to us right away?

I call you guys up quickly. We do a physical exam. We take the history that we know how to take. We’re not super comprehensive as you all are. You guys have scores that you go through and screening methodology more specifically. We do a little bit of protecting, an ASCA [anti-Saccharomyces cerevisiae antibodies] type approach or looking at biomarkers to discern whether or not there’s something that merits a quicker referral. We certainly ask about the usual questions of bowel movement frequency, hematochezia, abdominal pain, etc. And so, obviously, we have this ongoing and smooth collaboration between our centers that is very helpful to us as clinicians, but most importantly to our patients because we have this ongoing dialogue that’s helpful for clinical care.

Jordan, how do you ask about extraintestinal manifestations when you’re seeing somebody in the office? Because I think we all, including myself, don’t do as good of a job as we should.

I think that it’s probably underappreciated in the GI office. The actual magnitude of extraintestinal manifestations, in particular, the joint and skin manifestations of IBD are really underappreciated and I think we’re learning the right way to ask that. I learned from Jose that I should be asking about back pain, which I now ask specifically about in addition to just joint pain because you want to know about spondyloarthropathy and axial involvement and whatnot. That also influences how we think about the right medications and also the right types of doctors that they also need to see to be on the same treatment team as far as dermatology or rheumatology. Back pain has come into joint pain, and then, of course, I go into things like vision, skin, rash. Those are really the big ones.

I think that’s a great point. When we ask, when I first started, I would just say, do you have joint pains? Yes or no? Then they say, “No,” and then they’ll just bring it up later. I think we need to do a better job of asking these questions in the office because, as you just alluded to, it’s really going to affect our treatment decisions now that we have more therapeutic options, some that are more targeted, which might be good for 1 reason but maybe not as good for patients with extraintestinal manifestations.

Jose, let’s say I have a patient I asked about joint pains that said their knee hurts or their back hurts. What other questions should we be asking as gastroenterologists that could help us determine if this is something to call our rheumatologist about? Should we send other tests, or is it somebody that’s just ran a few miles or they’re getting older and it’s just a little wear and tear?

Really good question, Dave. Patients with diabetes, and similarly to those with spondyloarthritis or psoriatic arthritis, tend to be on the young side. Obviously, young is a relative term, at least for me it is. But we’re talking about patients in their 20s, 30s, and 40s and therefore you eliminate right away the wear and tear type of joint pain, osteoarthritis, and the like. You really want to focus on whether or not this pain is secondary to trauma or exercising. A lot of people, particularly in New York where we practice, are runners or do high-impact sports. You really want to know whether that’s a meniscal tear or if they’ve been having some other trauma or microtrauma that would explain that particular joint pain.

What we’re interested in are symptoms of pain in a specific joint that associate with swelling, for example. Swelling is a huge one. If you have swelling and pain, that’s more likely to be inflammatory in nature unless there was trauma to begin with. Redness and warmth are other signs leading towards a differential diagnosis of inflammatory disease. The third one could be a history of infection. Again, the Northeast and Lyme disease go together. So that’s a good question to ask. Have you been bitten by one of these bugs at all? Or any other infections, Caribbean-related trips where you have the viral syndromes like chikungunya, Zika virus, etc.? Beyond that, I think we want to make sure that there’s a screening process where not every joint pain equals inflammatory arthritis.

Jose, what do you think about the patients that come in and say, they wake up in terrible back pain or terrible joint pain and then throughout the day it starts to get better? Is that good enough to help differentiate between inflammatory and noninflammatory?

I would say yes, for the most part. Just for the record, what I was referring to before was peripheral arthritis … etc. Embedded in your question is, is this a lower back pain that’s inflammatory in nature? We indeed classify those as back pain that starts in the morning, typically in someone who is 40 years of age or younger that associates with morning stiffness of an hour or more. As you pointed out, typically it gets better or improves with mobility or exercise. Unlike, and the huge differentiating factor, is if you had a slipped disc or you had some sort of radiculopathy, where that pain is there constantly. No matter what you do, if you have a herniated disc you will not get any improvement with mobility. Actually, you may worsen that pain because the slipped disc will be in contact with the nerves that are being impacted by the slipped disc. So yes, those questions are very important.

The fifth point on discerning inflammatory back pain from noninflammatory back pain has come up recently, and that is the use of NSAIDs [non-steroidal anti-inflammatory drugs]. If a patient says that with NSAIDs they get better, then that’s more likely to be related to an inflammatory process. The challenge there is that the new data doesn’t necessarily show that. That improvement with NSAIDs is true for both inflammatory and noninflammatory pain. I don’t think we’re going to hold you guys accountable to that. And I will add that you don’t use that many NSAIDs in your patients anyway.

I think those are all great points and we need to do a better job taking that history. That’s just a couple of extra questions separating joint and back pains, asking is it better or worse with rest, and looking at their age. Then on physical exams, actually looking at the joint. Is it swollen and so forth? Let’s say we’re doing this in our office, the patient gets a little worse at rest and is better with exercise. Is this the right time to send them over to you? Should we be doing any other tests in the first place before sending them over to you? Is there a specific time that you think is best?

We’ve collaborated in some studies to try to understand how to screen inflammatory back pain in those kind of patients. I think that for the general practitioner this is a very straightforward and linear imaging test. I’m referring to sacroiliac [SI] joint x-rays, plain x-rays. The reason for that is that that’s very helpful. We’re going to do that no matter what in general. So if you have that patient whom you suspect inflammatory type back pain, you could help us and help the patient accelerate or expedite the workup by doing the x-ray. The reason for that is if we find any images that are representative of sacroiliitis, then we’re done. We say that patient has radiographic axial spondyloarthritis. So we’re done with the assessment.

I understand that it’s hard and you may not want to order the wrong x-ray, but this one in particular is very straightforward. It’s a dedicated sacroiliac joint x-ray. You can’t go wrong with that. Any radiologist would understand that order. Other than that, I think we can do a quick visit and then think about whether or not the next level of imaging studies are necessary, referring to the MRI.

Jose raises a good point about the MRI because our patients with Crohn’s disease in particular get these very often. Many of our radiologists may even comment on the SI joints and we may not be looking. As a gastroenterologist, we don’t really focus on the GI components, but that’s important.

 Jose, maybe you want to comment on this? We had a collaborative publication looking at exactly what Jordan’s saying. Looking at our MR [magnetic resonance] enterographies [MREs] that we have already for Crohn’s disease and actually going back and having our radiologists take a little closer look at the SI joints.

It was a fascinating study. That’s one of those where we made really good use of our collaborations. You guys do MREs. You look at the inflammatory component in the intestinal lumen, but as an add-on, you could look at the sacroiliac joints. It’s in the same area and it’s using MR technology. So we went back and found that somewhere in the order of 20% of the patients you see with Crohn’s disease will have MRIs consistent with sacroiliitis. It is a magnificent way of screening those patients for not necessarily clinically active or symptomatic but yet concomitant axial spondyloarthritis. That’s important because treatment is not necessarily the same, as you were alluding to, Dave. If you have a patient with Crohn’s disease with axial spondyloarthropathy, we have all these new biologic treatments that may or may not affect the spine, for example, or the peripheral joint.

It’s a great point. Now, from this study, our radiologist specifically comments on the SI joints in the report. It was sort of a request we had. Again, there are other tests you can do, but that’s something easy since you already have that information. You’re not spending more time in your office to get that.

Why don’t we pivot to that, Jose, looking at approaches to therapy. Start with psoriatic arthritis. When you’re thinking about treatment options for your patients, what would you go to regularly? Let’s take out IBD for a second and then we could bring that back in. Then, Jordan, let’s hear your thoughts on how we approach it with the concomitant diagnosis.

Great question. Similarly, to the IBD field, psoriatic arthritis patients present in a heterogeneous fashion. It’s not a linear one-size-fits-all therapeutic algorithm. To us it’s very important to understand the intensity or activity of the different domains. It’s not the same to treat someone who has a lot of psoriasis in their skin or someone with a lot of joints with little psoriasis.

I’ll take you through 2 or 3 scenarios. If you have a patient that presents to you with severe active psoriasis and peripheral arthritis, we tend to use a medication or a set of medications that can help both domains. By that, I mean an IL [interleukin]-23 blocker or an IL-17 blocker, because those are superior in some ways to the TNF [tumor necrosis factor] blockers when it comes to psoriasis of the skin. If you have a patient with mostly arthritis and little psoriasis, a TNF is the go-to mechanism for a variety of reasons. It has been for the last decade or decade and a half and would seem to me that it will continue to be the go-to MOA, or mechanism of action, because of the advent of biosimilars. Then we have patients that present, as we were discussing, with axial or spine arthritis. That complicates matters because there are not that many drugs or options. We’re limited to a TNF or an IL-17 blocker. After that we have the JAK [Janus kinase] inhibitors that are being approved for the use in axial or spondyloarthritis. So those are the 3 main scenarios. Purposefully, I didn’t comment on the presence or absence of IBD, but I’m hearing that you have some thoughts on that.

So, Jordan, let’s throw in IBD there with an extraintestinal manifestation, so skin or joint. How are you approaching those patients?

Sure. There’s a couple of really important considerations. What I’ll say is that in IBD we don’t have IL-17 inhibitors. Those have actually been associated with some flares of IBD, so we don’t have them as treatment options. But they are sort of academically interesting for patients who develop GI symptoms on these drugs. That’s almost a separate chat in and of itself.

Similar to what Jose said, a lot of times if there’s axial involvement with inflammatory bowel disease, anti-TNFs tend to be the therapy of choice that seem to benefit both. I think when there’s psoriasis present in psoriatic arthritis, in particular with peripheral arthritis, I think that’s a good indication for the IL-23, IL-12/23 inhibitors. That seems to have pretty good coverage. Now, if a patient has disease severity of their IBD that makes me want to use an anti-TNF or infliximab then I’m still going to use that in that patient, but I think we have some data that suggests IL-12/23 and IL-23s work really well for that patient. Then of course the JAK inhibitors, which are not yet approved in Crohn’s disease but are approved in moderate-to-severe ulcerative colitis, are another option for many of these folks.

The other really important scenario, and Jose it’d be great to get your feedback on this, are for the patients who develop psoriasis while they’re on IBD therapies. This is a different patient in and of itself. So not the patients who come to you treatment naïve with joint pains, new diagnosis of ulcerative colitis, or Crohn’s disease, but the patients who we already have on therapy who now develop a skin manifestation. What are you thinking about?

That’s a great question. It depends on what the background regimen is. We do this all the time at both of our centers. It really is dependent on what the patient has been treated with. In general, that may occur for 2 reasons. One, the medication that’s being used stopped working. Two, something to consider is the paradoxical effects of TNF blockers, for example. We have those patients commonly. It’s not hyper frequent but it’s there. So you have to consider the possibility that some of these patients develop psoriasis secondary to using a TNF blocker. In those scenarios, whether there’s a secondary inadequate response or there’s a paradoxical emergence of psoriasis, we do switch medications or try and think first of using an IL-23 or an IL-12/23 in the absence of axial arthritis. So with peripheral arthritis, for example, or no arthritis at all, but when a patient with IBD on a TNF blocker develops psoriasis we tend to switch to IL-12/23 for obvious reasons. IL-12/23 or IL-23 blockers are exceedingly efficacious in psoriasis. We all know that. And so because they work as well in IBD, then that’s the immediate answer. Could you switch from 1 TNF blocker to the next? Yes, you could. We typically avoid that though. We switch drug classes.

I think it is interesting. Earlier literature for IBD, before we had ustekinumab and risankizumab or IL-12/23, and IL-12 and IL-23, we would switch. Maybe certain TNFs had lower rates of reaction to having another psoriasiform reaction, but it’s still a chance. Jose, briefly comment on how does that psoriasis usually present? Is it differently than a regular psoriasis if it’s from a TNF blocker?

Paradoxical psoriasis more frequently presents as either palmoplantar psoriasis. It’s not infrequent. It could present as plaque or guttate psoriasis, but its the minority of cases. When we get a hint that someone who either never had psoriasis to begin with or had a different type of psoriasis now presenting with palmoplantar lesions, we tend to suspect that that’s paradoxical in nature.

That’s a great point. We are discussing the difference between IL-23 and an IL-12/23. We don’t have great data yet to say that one is necessarily better than the other. They’re equivalent. In rheumatology, do you lean towards one over the other? So would you lean towards an IL-23 inhibitor over ustekinumab, and why?

Unlike the IBD field, we moved away from the IL-12/23. Rheumatologists and the dermatologists as well. It is simply a P19 blocker. A pure IL-23 is simply superior for skin and joints. There’s data for both, more for skin than there is for joints. We actually never used that drug. There’s only one in the market. I don’t think we’ve ever actually used that drug the way you or the dermatologists have. If you ask the company they will tell you that the rheumatologist never went there. And it’s true that the joint response for IL-12/23 is not robust. There are patients that are on it and respond well, but majority won’t. So that’s why we like the P19s now.

Up until recently we only had ustekinumab in our field and now we have risankizumab that obviously brings something different to the table. I guess one of the more challenging things for us, Dave, and it’d be good to get your perspective, is when we have a patient who’s had very severe disease of their IBD and are finally well controlled on maybe a dose-escalated anti-TNF therapy, who now develops a psoriasiform reaction. Is that someone that you think about switching therapies, adding therapies, or what do we do here?

Great point. I would say most of the time the IBD disease burden is more of a significant inflammatory burden than the joint or the skin. If we’re saying that this is a sick patient that failed multiple therapies, maybe had past surgery, or whatever that is, it’s all about efficacy and keeping them in remission. So if I found a therapy that’s working for them and they’re doing well from their IBD perspective, my goal is to keep them on it.

Now, what is the severity of that psoriasiform reaction? Usually if they’re doing well on something, if they could be treated with topical medications or where you could have these mild reactions, I’m keeping them on their TNF. I need to be pushed, and this is my view on a lot of our patients with IBD, especially our more complex patients. If I have them well on something, I really need to be pushed to stop. I’ve had these patients with that exact scenario where they have significant scalp psoriasis and I have to get them off of it, then we’ll talk about it. But in those scenarios, I do whatever I can to stay on the TNFs and then depending on the severity, those are the patients where I think JAK inhibitors are going to play a nice role. We do need some more data on that, but that’s where I think we might lean towards to cover both.

If I may interject, I think it is exactly what you’re saying for the burden of inflammation. We do the same in arthritis. When a patient failed so many other drugs in the past and we finally got them under control, we typically don’t switch that medication at all. The dermatologists, our friends and colleagues, have multiple tricks that they can use. There are topical medications, UV [ultraviolet] light, a little bit of cyclosporine. There’s plenty of things that they can do.

I’m not going to talk about clinical management, but there are clinical trials ongoing where the question is, in patients particularly early in the game, is there a role for combining with the second targeted agent? And again, for the sake of this discussion, this is not clinically available. But a study such as VEGA, which you guys know very well, combining a TNF with an IL-23, or in our case, we have a similar design in the trial that is called AFFINITY. This study is on someone who fails a TNF with the additional IL-23 in psoriatic arthritis. Will it be better than an IL-23 alone to switch to an IL-23? So intriguing times. Those secret patients are important for that particular reason. It may very well be that we get to a combination on those that need it the most.

We’ve had a lot of discussion on combination therapy just in our practices and how we use them, and EIMs I think is a perfect scenario where we are starting to do that by necessity. But I think we need to be more thoughtful in how we use combination therapies. Then something you had just brought up about how we haven’t really seen that benefit in the IL-12/23s for joints. What’s your experience with the selective IL-23 inhibitors with joint symptoms, joint swelling, and so forth?

 It’s a step up compared to an IL-12/23. It really is, the clinical trials show that. Early use compared to a second-line use doesn’t really make a difference. That’s also an advantage. You can use it a second-line and it’s still efficacious. The downside is the spine, as discussed, it doesn’t seem to work on the spine, and therefore we avoid the use of pure IL-23s in those scenarios.

Great. I just want to get your final thoughts on if we’re seeing a patient, when we should refer? If you are seeing a patient, when do you reach out to us? It really sounds like from everything we’re discussing, from IL-17s possibly leading to flares of Crohn’s disease, to side effects of certain medications of our therapies, to the selectivity of our therapies, we should do this before we start. But how does this workflow usually work in your practice?

In general, to me the key here is to have a fluent, fluid, smooth relationship and communication channel open with you guys and the dermatologists. Where you could truly either pick up a phone or send a MyChart note and say, “Here’s a scenario. Can I take 3 minutes of your time? I’ve done fecal calprotectin and it’s borderline. Do you think you want to see this patient, or do you want to wait?” I think that communication is missing in some geographic regions. The more we can do to incorporate those channels of communications to other practices the better for our patients.

Secondly, I think educating on the role of combined care will be very important. Embedded into that is the question of screening. What can we do to help screen for IBD? What can you do in the IBD world to screen for joints? What will we discuss? A third component here is forensic dermatologist, because we have these other EIMs that are so relevant to our patients. By the way, the patients are an N-of-1. They’re their own statistics. So if you only treat the gut, or the joints, or the skin, then we’re losing time, we’re not communicating, and we’re not making anybody any favor.

I think the collaboration is really key and working with the team of course. I think as gastroenterologists it’s important that we recognize our limitations. We’re not dermatologists. We’re not rheumatologists, and so it’s not good enough if patients are really struggling despite being on a therapy that we think is directed for their IBD. If they’re still experiencing active psoriasis or active joint symptoms, then they really need to have expert referral and collaboration to improve care.

I think those are all great points. Early collaboration is key. Finding those people in your area that you could reach out to that you could text or email on thoughts. I think what we could do better as gastroenterologists is just a couple of simple things. Asking those questions about skin, about timing of when these skin or joint symptoms started around medication. Asking that separate question between joint and back pains. Asking about whether that pain is better or worse with rest and exercise. Asking our radiologists to sort of take another look at the MRE at these SI joints. These are very simple things we could do as gastroenterologists that could really help hopefully diagnose or at least take these patients and get them over to rheumatologists so Jose and this team could help out. But I want to thank you, Jose, for joining us. This is a great discussion and we’ll see you soon.

Videos

Dr David Hudesman, Dr Jordan Axelrad, and Dr Jose Scher discuss strategies for managing coexisting inflammatory bowel disease and psoriatic arthritis and highlight the importance of a multidisciplinary approach to providing comprehensive care.

Concurrent Management of Inflammatory Bowel Disease and Psoriatic  Arthritis

To watch the video series component of this episode, click here.

Jose Scher, MD

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