Inflammatory bowel disease (IBD) and joint diseases such as spondylarthritis (SpA) are familiar comorbid conditions. But comorbid does not necessarily mean co-treatment, at least not with the rapidly developing armamentaria available to rheumatologists and gastroenterologists.
“Patients with IBD often come to the rheumatologist for their musculoskeletal symptoms,” said Dirk Elewaut, MD, PhD, Professor of Medicine and Principal Investigator at the VIB Center for Inflammation at Ghent University, Belgium.
“Rheumatologists tend to see this as classic spondyloarthritis but can forget that these patients have already been treated by a variety of drugs. They have already been on steroids, immunosuppressants, even biologics, which changes both the clinical presentation and diagnosis. MRI imaging, for example, can become much more difficult to interpret when the patient has already been treated for IBD.”
Dr. Elewaut will discuss some of the key points in treating patients who have joint problems with coexisting IBD and SpA during What Every Rheumatologist Should Know About IBD from 1:00 – 2:00 pm Monday in Room B304-B305, Building B in the Georgia World Congress Center. David Rubin, MD, the Joseph B. Kirsner Professor of Medicine at the University of Chicago, will focus on gut issues.
“We have more therapeutic options than ever before in IBD,” Dr. Rubin said. “And for the first time, we have therapeutic options that are not being used in rheumatologic conditions. The divergence in focus on the bowel compared to the joints is an important consideration for all of us.”
Because IBD and SpA are both inflammatory conditions, clinicians have long assumed that treating one condition will also benefit the other. Anti-TNF monoclonal antibodies work well in both gut and joints, for example, but there is a growing disconnect between gut and joints when it comes to newer agents that are more selective or have novel modes of activity.
Vedolizumab and other agents in development that are gut-selective do not cross-react with immune components in the joints or other parts of the body, Dr. Rubin noted. The lack of cross-reactivity has both advantages and disadvantages compared to older treatments that can affect both gut and joints.
“As we get more selective in just treating the bowel, we are either identifying patients who have some shared pathogenic processes that affect the joints but weren’t known or uncovering what was an otherwise treated joint problem that is no longer being helped,” Dr. Rubin said.
The disconnect between treatment effects in gut and joints works both ways.
“Drugs that work very well on the skin like IL-17 inhibitors should not be used in patients who have active IBD,” Dr. Elewaut cautioned. “There are agents like IL-23 inhibitors that are very useful in IBD but don’t work on the spinal inflammation we see in spondyloarthritis. And there is a fraction of patients in whom vedolizumab works very well in the context of IBD but can induce new onset joint symptoms.”
Simply having IBD can affect the effectiveness of some agents. An inflamed bowel changes the pharmacodynamics of some, but not all, agents used to treat joints and bowel.
“It is important that we all remember that patients leak protein from an inflamed bowel wall and, therefore, protein-based therapies don’t always reach therapeutic levels,” Dr. Rubin said. “That includes all of the monoclonal antibodies. The agents leak into the stool, and you may not be getting enough into the patient to have the needed therapeutic effect. The very real need to consider therapeutic drug monitoring or small molecule strategies that do not rely on proteins is something rheumatologists have to come to terms with. A leaky gut is not something that most people think about when they’re focused on managing joints.”