Lactose malabsorption is not always associated with intolerance symptoms. The factors responsible for symptom onset are not yet completely known. As differences in visceral sensitivity may play a role in the pathogenesis of functional symptoms, we evaluated whether an alteration of visceral sensitivity is present in subjects with lactose intolerance. Thirty subjects, recruited regardless of whether they were aware of their capacity to absorb lactose, underwent an evaluation of intestinal hydrogen production capacity by lactulose breath test, followed by an evaluation of lactose absorption by hydrogen breath test after lactose administration and subsequently an evaluation of recto-sigmoid sensitivity threshold during fasting and after lactulose administration, to ascertain whether fermentation modifies intestinal sensitivity. The role of differences in gastrointestinal transit was excluded by gastric emptying and mouth-to-caecum transit time by (13)C-octanoic and lactulose breath tests. Lactulose administration induced a significant reduction of discomfort threshold in subjects with lactose intolerance but not in malabsorbers without intolerance symptoms or in subjects with normal lactose absorption. Perception threshold showed no changes after lactulose administration. Severity of symptoms in intolerant subjects was significantly correlated with the reduction of discomfort thresholds. Visceral hypersensitivity should be considered in the induction of intolerance symptoms in subjects with lactose malabsorption.

Fasting and postprandial hypersensitivity characterize PDS patients and a reduction of gastric compliance is present in EPS patients. However, the pathophysiology of EPS appears more complex than PDS and further studies are needed to analyze central processing and integration of afferent pathways in order to clarify the role of the central nervous system in this condition.

No abstract

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.

No abstract