Colonic hypersensitivity is a major determinant of the efficacy of bloating treatment in constipation-predominant irritable bowel syndrome.

The pathophysiology of bloating is largely unknown, and many mechanisms have been proposed. An alteration of intestinal gas production may have a role in a subgroup of patients, but available data are conflicting. We have previously shown that hypersensitivity to colonic fermentation is associated with severe bloating in a subgroup of patients with low intestinal gas production. Accordingly, we evaluated whether modification of intestinal gas production improves bloating severity according to the presence of visceral hypersensitivity to colonic fermentation. Twenty-four IBS-C patients with severe bloating underwent intestinal gas production measurement by hydrogen breath test after lactulose, and a recto-sigmoid barostat test in order to evaluate sensitivity thresholds in a basal condition and after induction of colonic fermentation. The subjects were then randomly assigned to receive either rifaximin or placebo according to a double-blind, randomized, cross-over trial. Rifaximin induced an improvement of symptom severity. A post hoc analysis according to the presence of hypersensitivity to colonic fermentation shows that rifaximin induces a significant improvement in symptom severity only in normosensitive, hyperproducer patients. Modulation of colonic flora, in order to reduce fermentation, does not interfere with bloating severity in patients with visceral hypersensitivity, thus suggesting that in this subgroup of subjects gas production is not crucial for the onset of bloating.