Is Chronic Pain an Extraintestinal Manifestation of IBD? I nflammatory bowel disease (IBD) patients can have severe abdominal pain for many reasons including inflammation, obstruction, abscesses, and fistulae. The perception of pain will vary considerably in our IBD patients, with some patients being hypersensitive and others insensitive to painful stimuli. The challenge for the physician is how to adequately treat chronic pain without leading to long-term narcotic dependency. However, a significant percentage of our patients are on chronic narcotics, despite having an excellent response to medications or being in remission. Of great concern is that the chronic use of narcotics can conceal complications of IBD such as perforation or abscess formation, and has been found to be associated with toxic megacolon, increased rate of infections, and increased mortality. 1 Thus, we need to learn more about why our patients have pain and how to better treat pain in our patients. In this issue of Inflammatory Bowel Diseases, 2 articles address the important subject of chronic pain in IBD.
Hanson et al 2 examined the records of 100 IBD patients receiving narcotics. Narcotic use was found to be higher in women than men, increased in IBD patients who had had greater than 2 surgeries, associated with both moderate to severe pain and also disease activity, increased in IBD patients with depression, anxiety, and a history of abuse. The authors found that narcotics were able to be discontinued in IBD patients who were adherent to their treatment regimen and IBD patients who had lesser amounts (little or none) of pain and disease activity.
Bielefeldt et al 3 provide an overview of our current understanding of the cause of pain in IBD. They point out that a majority of IBD patients will experience pain during flares, but also note that up to 20% of patients in remission will continue to have significant pain. The authors review experimental animal data regarding lower thresholds of stimulus response and the idea of peripheral sensitization observed during visceral inflammation due to increased neuronal excitability and enhanced release of mucosal signals. They suggest that similar mechanisms may be at work in human IBD, and review potentially modifiable pathways for future treatment approaches. In addition, the association between pain, stress, and anxiety are discussed, leading to the importance of identifying coexisting psychiatric disease.
What these 2 articles teach us is that there are sub-groups of patients who are at risk for chronic pain, and that chronic pain may be a marker of more severe disease or underlying psychosocial difficulty. Chronic pain (predominantly abdominal or joint pain) is unfortunately a part of the management of patients with IBD, and the insights from these authors provide a framework of how to approach to this difficult problem.