Dr Rubin discusses how using a treat to target approach can enhance patient quality of life, achieve tight control of inflammatory bowel disease, and ensure optimal outcomes.

David T. Rubin, MD, is the Joseph B. Kirsner Professor of Medicine, chief of Gastroenterology, Hepatology and Nutrition, and director of the Digestive Diseases Center at the University of Chicago.

TRANSCRIPT:

Hi, I'm David Rubin from the University of Chicago. At the AIBD Regional Meeting in Chicago, this weekend, I spoke about the emerging use of treat-to-target in inflammatory bowel disease. This is a strategy where we acknowledge that, in order to control the disease, we should be working towards not just symptom improvement, which is really important and obviously related to improved quality of life, but also to objective targets that confirm that we've actually controlled the disease process.

And in IBD, we know for example, that patients with ulcerative colitis who feel well may have inflammation by scope or biopsy up to 50% of the time. And similarly in Crohn's disease, we can see very disparate outcomes based on just symptoms compared with objective measures of inflammation. So the treat-to-target strategy, which we've adopted and modified from rheumatoid arthritis and from other conditions like hypertension, diabetes, or asthma, has to do with the principle of identifying a reliable biomarker that is benchmarked to the disease activity at the time you diagnose a patient, and then choosing a therapy based on how sick they are and what their prognosis is for poor outcomes.

And then after starting that therapy, assessing that same biomarker in some way to know whether or not you're gaining control of the inflammatory process. The other part of treat-to-target that's critically important is a shared decision-making conversation between the provider and the patient to make an adjustment to the therapy if the target isn't reached.

What we've learned about treat-to-target in inflammatory bowel disease over the last number of years are a number of important points. The first one is that when we assess to know if a treatment is working can be at a shorter interval than we previously thought. We used to say, assess it 3 to 6 months. That might be too long for a therapy that you've just started, which should be working rapidly. And you should have a good sense that it's getting you where you need to go. In fact, with some of our newer therapies, we see that they work within days in many cases. And remission may be obtained within a couple of weeks. So it's reasonable to start by shortening the interval in which you reassess the target.

The second message has been we've learned a lot more about how clinically we might do better at attaining and achieving our targets. And what I mean by that is that includes treating earlier in the disease process to get people on therapies that are going to have a greater likelihood of working. And secondly, we've learned a bit more about how to sequence therapies and what to do when one drug isn't working or loses response.

Now, sometimes, we think of this as being just a practical matter. What's the next drug we would consider, and what's available from our payers? But other times, it's actually starting to emerge that there can be some biological principles to guide us in choosing therapies as sequences in treat-to-target.

What I mean by that would be a patient, for example, who is on an anti-TNF therapy for their Crohn's disease but develops a skin problem like TNF-related psoriasis; well, in that case, we've learned that that's probably associated with an activated IL-23 pathway. So when you consider a second therapy in that specific scenario and you're working towards a treat-to-target management strategy, you would then choose a drug that might target IL-23 as its primary mechanism.

Another example might be thinking about a comorbid or coexisting other immune problem. Imagine a patient with Crohn's or colitis who also has joint pain, for example. What we've learned a lot more about how joints and the bowel are related, and this is not necessarily overall new, but we've learned certainly are that there are certain therapies that might work better for the joints.

IL-23 and anti-integrin therapies don't really get at joints unless it's specifically related to the bowel itself driving it. But what we do know works when you have joint problems are the JAK inhibitors and anti-TNF. So you can think about what treatment would I use in sequence if I have a patient who has one of these extraintestinal manifestations as a clue as to what might be a unifying inflammatory pathway for that patient's multiple problems.

As you move through therapies with treat-to-target, you can start being thoughtful about which treatment to use and in which patient we should try them. And I think that, overall, we could be achieving a lot higher remission rates if we communicate effectively, if we assess earlier, if we have identified and benchmarked biomarkers for individual patients. And then, we're thoughtful about inflammatory pathways, coexisting extraintestinal manifestations, and how to sequence therapies in a meaningful way.

We're making a lot of progress with emerging evidence supporting the strategy. And I'm sure that you can be incorporating this into your practice in a meaningful way going forward. I hope that this has been helpful. I'm sorry I didn't get to see you in person at AIBD Chicago, but I look forward to seeing you at future meetings.