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The nature and clinical implications of irritable bowel syndrome (IBS)-type symptoms in patients with inflammatory bowel disease (IBD) who are in apparent remission have generated considerable debate. While, on the one hand, these symptoms satisfy Rome III criteria for IBS and their occurrence correlates highly with anxiety, a known trigger for IBS, on the other hand, recent studies have shown that many of these patients exhibit subtle inflammatory changes. Are these symptoms ‘true’ IBS superimposed on IBD, or an active but sub-clinical form of IBD? We propose a unifying model to explain and reconcile current knowledge on this topic, a model that could provide a conceptual framework for understanding the nature of these symptoms and point towards effective management strategies. We propose that IBS symptoms in IBD patients who are in remission be termed irritable inflammatory bowel syndrome in order to emphasize their unique presentation and etiology and to distinguish them from both IBS and IBD.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Key issues
The occurrence of irritable bowel syndrome (IBS) symptoms in inflammatory bowel disease (IBD) patients who are in remission is a significant problem for both patients and clinicians as it presents a diagnostic and treatment conundrum. On the one hand, untreated intestinal inflammation can lead to a full-blown relapse of IBD, and, on the other, overtreatment of innocuous IBS symptoms may lead to decreased quality of life and increased morbidity.
What is the pathophysiological nature of these symptoms? Do these symptoms in all patients necessarily entail intestinal inflammation, or may there be the subset of IBD patients who have IBS symptoms without significant inflammatory features? Can we use inflammatory markers, such as calprotectin, to differentiate these two patient populations?
We propose a new interpretation of current data that has the possibility of explaining available observations and provide a unified theoretical model for understanding IBS-like symptoms in IBD. We argue that IBS symptoms in IBD necessarily entail a degree of inflammation that may, or may not, be significant enough to be detected by fecal assays for calprotectin. We recommend that calprotectin be used to identify the patient population that requires further testing to identify occult, but ongoing, IBD activity and more aggressive anti-inflammatory therapy.
We suggest that IBS symptoms in IBD patients who are in clinical remission be viewed as a new syndrome separate from both IBS and IBD. In this way, we will be better able to understand the relationships of these subjects to both IBS and IBD and to develop diagnostic and treatment strategies that would be better tailored to this patient population.