Letter: the role of sub-clinical inflammation and TRPV1 in the development of IBS-like symptoms in ulcerative colitis in remission

We read with interest the article by Berrill et al.1 In their study, the authors addressed the potential role for sub-clinical mucosal inflammation as a cause for irritable bowel syndrome (IBS)-like symptoms in patients with inflammatory bowel disease (IBD) in remission. The authors demonstrated that faecal calprotectin levels, indicators of mucosal inflammation, were comparable in IBD patients with or without IBS-like symptoms. A recent study by Jonefjäll et al.2 investigating 94 patients with ulcerative colitis (UC) in remission came to the same conclusion. These findings are in contrast to the findings of Keohane et al., who observed significantly higher calprotectin levels in IBD patients with IBS-like symptoms.3 In support of the findings of Berrill et al. and Jonefjäll et al., we were also unable to demonstrate a significant difference in calprotectin levels among 36 UC patients in remission, both with and without abdominal pain, reflecting IBS-like symptoms (see Figure 1). However, in UC patients with abdominal pain, faecal calprotectin levels significantly correlated with pain scores (r = 0.80, P = 0.002). Furthermore, we demonstrated increased transcription of the nociceptive signalling molecule TRPV1 in this group, which also correlated with pain scores.4 This is in line with the findings of Akbar et al.5, who demonstrated that UC patients in remission complaining of abdominal pain had significantly higher numbers of TRPV1-positive nerve fibres in the rectosigmoid mucosa. We therefore hypothesise that the potential cause of IBS-like symptoms in UC patients in remission is not the sub-clinical inflammation per se, but rather the secondary changes induced during the acute inflammatory phase, which persist during remission. Upregulation of TRPV1 could represent one of these secondary alterations in mucosal neurobiology responsible for increased peripheral nociceptive discharge and subsequent pain symptom development. The reason why this occurs in only a fraction of UC patients in remission remains to be elucidated. Declaration of personal and funding interests: None.