Letter: irritable bowel syndrome-type symptoms in paediatric inflammatory bowel disease.

Abstract

We read with interest the article by Diederen et al. investigating the relationship of irritable bowel syndrome (IBS)-type symptoms and biochemical markers of disease activity in inflammatory bowel disease (IBD).1 The authors found that IBS-type symptoms in children with IBD appeared to be unrelated to gastrointestinal inflammation. As their findings are different from previous studies, this may lead to uncertainty in management of these patients. Therefore, this issue deserves further discussion. First, the physician-administered Rome III-questionnaire was used to determine the presence of functional gastrointestinal symptoms compatible with Rome III criteria for IBS in this study. The absence of an objective biomarker for diagnosing IBS has meant that studies examining the phenomenon of IBS in IBD patients have used symptom-based criteria to define its presence. As a result, it is unclear whether this is “true IBS” or whether there are common pathophysiology causing similar symptoms that simply meet the criteria for a diagnosis of IBS. Second, some studies have demonstrated that the levels of faecal biomarkers of mucosal inflammation, such as calprotectin, have been shown to be elevated in IBD patients in clinical remission with IBS-type symptoms, suggesting that subclinical inflammation or subclinical disease activity is the cause.2, 3 In this study, biochemical remission was defined as a faecal calprotectin (FC) level <250 μg/g. However, previous studies have demonstrated that there is a much higher proportion of patients with IBS-type symptoms who have mildly elevated FC levels (100–200 μg/g), and it is feasible that this low level of inflammation may account for the symptoms experienced in these patients.4 At the same time, it may also be necessary to define more sensitive methods to detect occult inflammation in these patients. Third, some studies implicate increased paracellular permeability as a potential cause for the development of IBS-type symptoms in IBD patients with clinical remission, and highlight the fact that its development may be secondary to ongoing occult inflammation, increased inflammatory cell infiltrate, and increased proinflammatory cytokine expression, rather than true functional bowel disease coexisting in IBD patients with clinical remission.5 At the same time, the limited correlation between symptoms and actual mucosal inflammation has been highlighted in many studies, and emphasises the importance of using objective markers of inflammation to manage IBS-type symptoms in IBD patients in clinical remission. Future studies should explore the relationship of IBS-type symptoms with novel biochemical markers of disease activity in IBD patients with clinical remission. Declaration of personal and funding interests: None.