Chronic Abdominal Pain
For up to 50% of people with IBD, abdominal pain is a constant companion, and the currently available remedies aren’t always helpful and can even be harmful.
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or aspirin, can cause gut bleeding. And opioids, the strongest type of medicines available to treat pain, are often addictive and may cause additional discomfort by triggering constipation.
To address patients’ pressing needs for reliable relief, we recently launched the Chronic Abdominal Pain in IBD initiative. Through this, we’re now funding three studies that may help to answer some key questions about the underlying biology of this pain and why certain patients are more likely to suffer from it.
Some questions we’re hoping to answer via this initiative include:
Why doesn’t IBD remission always result in pain relief?
It’s easy to understand why flares can be painful. Yet about half of patients who go into IBD remission (defined as no longer having objective evidence of gastrointestinal inflammation) continue to struggle with chronic abdominal pain. To understand why, we need to know what’s going on in the gut as well as in the brain, which is where pain sensations are processed.
Using a grant from the Foundation, Qasim Aziz, PhD, of Queen Mary University of London, is recruiting 300 IBD patients. He will follow them for several years and compare what’s happening in the brain, intestines, and microbiome (gut microbes). His aim is to identify what’s different in these areas for people whose pain resolves after a flare as compared to those whose pain becomes chronic.
Is an enzyme connected to chronic abdominal pain?
Thanks to funding from our IBD Ventures program, Barbara Slusher, PhD, director of the Johns Hopkins Drug Discovery program, has been studying a drug-like substance that can block an enzyme called GCPII, which is dramatically higher in IBD patients with inflammation. Now, using a grant from our new Chronic Abdominal Pain Initiative, she will attempt to determine whether GCPII stays elevated in people with chronic abdominal pain.
Her hypothesis is that GCPII increases during an IBD flare and makes neurons (nerve cells) more excitable, so they respond more readily to pain—and that these neurons remain activated even after the inflammation has eased off. In addition to studying about 120 patients at Johns Hopkins, she will be tapping into data from IBD Plexus, the Foundation’s massive data platform, which includes a linked biobank (a collection of biological samples, such as blood, stool, and intestinal cells).
Could bacteria and fats in the gut be causing chronic pain?
At McMaster University in Canada, Premysl Bercik, MD, PhD, has been studying lipids (fats) in the guts of people with IBD as well as in those with irritable bowel syndrome (IBS), a condition that’s characterized by unexplained abdominal pain. He has already determined that a subset of patients with IBD or IBS (or both) have high levels of specific lipids in the gut.
These fats are produced by gut bacteria after a person eats certain foods. If Dr. Bercik and his colleagues can pinpoint which bacteria are responsible, people with high levels might be able to ease or do away with their pain simply by making changes to their diet.
