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David Rubin, MD, on De-escalating Treatment for IBD
Dr Rubin reviews his recent presentation from the American College of Gastroenterology 2020 clinical meeting and postgraduate course on why, when, and how to de-escalate or discontinue various therapies for the management of ulcerative colitis and Crohn disease.
David Rubin, MD, FACG, is chief of gastroenterology, hepatology, and nutrition and codirector of the Digestive Diseases Center at UChicago Medicine.
Transcript
Hello, I'm Dr. David Rubin from the University of Chicago. At the American College of Gastroenterology annual meeting this year, which is virtual for the first time, I am speaking on the postgraduate course on de-escalation of therapies in inflammatory bowel disease.
This is an important topic, not just because our patients frequently ask when they can stop their therapies, but in considerations of costs of therapies, long-term exposures of therapies, and in the chronic management of a condition like Crohn's disease or ulcerative colitis, deintensification or de-escalation of therapies is something that we should be knowing more about.
In my presentation, I review the general strategies for approaching this complex topic as well as the importance of communicating effectively to your patients about what is realistic and what we need to do to consider it.
In general, the evidence for de-escalation exists to support reducing the intensity of our therapy in patients who have achieved stable remission for at least six months or a year. A classic example of this that you all know about is when we use steroids to induce remission.
Of course, we then move to a steroid-sparing maintenance strategy. We remove the steroids as a way to de-escalate in that situation. We have in fact learned how to do this effectively by using markers of active disease.
For example, knowing that a fecal calprotectin has normalized or near normalized tells us that is safe to rapidly remove steroids. Thinking about our other therapies, we have to consider what the evidence says as well as the practical reality that we haven't cured IBD yet.
We have some data that exists that suggests that, for example, inducing remission with higher doses of mesalamine can be safely reduced to a lower dose of mesalamine when the patient has achieved mucosal healing or at least endoscopic improvement of their bowel. This was published in a phase 4 open-label study, and I review the data in my postgraduate presentation.
Considering our biological therapies, as well as immunomodulators, we have additional data that suggests that patients who have achieved remission and are in stable, deep remission for at least 1 year might be candidates for the removal of the immunomodulator, provided that you accurately measure the drug level before you do so and know what is likely to happen to the biologic therapy after an immunomodulator is discontinued.
For example, the biological therapies of anti-TNF will have a drop in their level when you remove the thiopurine or the methotrexate that's being used in combination. An important strategy to any de-escalation plan is monitoring your patient after you do so.
Monitoring includes assessing their symptoms, but better than that is to use biochemical markers or stool markers which will predate clinical relapse. You'll know then that the patient is already starting to have a problem, and you should have a rescue strategy in place.
In my presentation, I review all of these data as well as some general recommendations, and I think it's a practical approach to this very common scenario. Thank you.