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IBS continues to evade the efforts of medical science to translate knowledge of putative pathogenetic or pathophysiological mechanisms into successful pharmacological treatments. To some extent, laxatives and antidiarrhoeal medications are able to improve the erratic bowel habits associated with IBS, and recently linaclotides have been shown to relieve abdominal pain and constipation in IBS-C.1 Even so, in those experiencing treatment success this cannot be linked to a disease-modifying effect, since stopping the treatment leads to recurrence of symptoms.
From this point of view, a hot topic during the past decades has been the many reports of low-grade immune activation in subgroups of patients with IBS.2 The early observations of GI infections as a risk factor for developing IBS,3 but also other functional GI disorders such as functional dyspepsia,4 has sent signals of hope for anti-inflammatory treatment as a promising approach for a subset of patients. Epidemiological observations of a reduced risk for IBS in users of oral steroids pointed in the same direction.5 The lack of a positive effect of prednisolone treatment in postinfectious IBS, except for reducing the number of lamina propria lymphocytes,6 was disappointing but has not hampered the conceptual interest. Instead, it has rather focused efforts into medications with a better possibility for long-term treatment such as the mast cell stabiliser ketotifen7 and even more interesting, 5-aminosalicylic acid in the form of mesalazine8 that might affect …