Role of colonic fermentation in the perception of colonic distention in irritable bowel syndrome and functional bloating.
ABSTRACT Bloating represents a frequent gastrointestinal symptom, but the pathophysiologic mechanism responsible for its onset is still largely unknown. Patients very frequently attribute the sensation of bloating to the presence of excessive bowel gas, but not all patients with gas-related symptoms exhibit increased intestinal production of gas. It is therefore possible that other still unrecognized mechanisms might contribute to its pathophysiology. Our aim was to evaluate whether a subgroup of patients affected by functional abdominal bloating presents hypersensitivity to colonic fermentation.
Sixty patients affected by functional gastrointestinal disorders (11 functional bloating, 36 constipation-predominant, and 13 diarrhea-predominant irritable bowel syndrome) and moderate to severe bloating took part in the study. Twenty sex- and age-matched healthy volunteers were enrolled as a control group. All the subjects underwent a preliminary evaluation of breath hydrogen excretion after oral lactulose. Then, on a separate day, an evaluation of sensitivity thresholds at rectal level was performed with a barostat before and after the induction of colonic fermentation with oral lactulose. A control test with electrolyte solution was also performed.
Both breath hydrogen excretion and mouth-to-cecum transit time did not differ between the 4 groups studied. Neither electrolyte solution nor lactulose modified sensitivity thresholds in healthy volunteers. In low hydrogen producers, basal perception and discomfort thresholds were similar to high hydrogen producers, but after lactulose both perception and discomfort thresholds were significantly reduced only in low hydrogen producers.
A subgroup of patients with functional gastrointestinal disorders and moderate to severe bloating might have hypersensitivity to products of colonic fermentation.
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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.Internal and Emergency Medicine 12/2010; 6(5):403-11. · 2.35 Impact Factor
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ABSTRACT: BACKGROUND: The association of fructose and lactose intolerance and malabsorption with the symptoms of different functional gastrointestinal disorders (FGID) remains unclear. AIM: To investigate the prevalence of fructose and lactose intolerance (symptom induction) and malabsorption and their association with clinical gastrointestinal (GI) as well as non-GI symptoms in FGID and the outcome of dietary intervention. METHODS: Fructose and lactose intolerance (defined by positive symptom index) and malabsorption (defined by increased hydrogen/methane) were determined in 1372 FGID patients in a single centre using breath testing. Results were correlated with clinical symptoms in different FGID Rome III subgroups. The effectiveness of a targeted saccharide-reduced diet was assessed after 6-8 weeks. RESULTS: Intolerance prevalence across all FGIDs was 60% to fructose, 51% to lactose and 33% to both. Malabsorption occurred in 45%, 32% and 16% respectively. There were no differences in intolerance or malabsorption prevalence between FGID subgroups. FGID symptoms correlated with symptoms evoked during testing (r = 0.35-0.61. P < 0.0001), but not with malabsorption. Non-GI symptoms occurred more commonly in patients with intolerances. Methane breath levels were not associated with constipation using several cut-off thresholds. Adequate symptom relief was achieved in >80% of intolerant patients, irrespective of malabsorption. CONCLUSIONS: Fructose and lactose intolerances are common in FGID and associated with increased non-GI symptoms, but not with specific FGID subtypes. Symptoms experienced during breath testing, but not malabsorption, correlate with FGID symptoms. Effective symptom relief with dietary adaptation is not associated with malabsorption. Mechanisms relating to the generation of GI and non-GI symptoms due to lactose and fructose in FGID need to be explored further.Alimentary Pharmacology & Therapeutics 04/2013; · 4.55 Impact Factor
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ABSTRACT: Irritable bowel syndrome patients with diarrhoea (IBS-D) often report intolerance to milk; however, the mechanism underlying these symptoms is unknown. To assess the role of psychological factors, immune activation and visceral sensitivity on the development of lactose intolerance (LI) in IBS-D patients. Fifty-five IBS-D patients and 18 healthy controls (HCs) with lactase deficiency underwent a 20-g lactose hydrogen breath test (LHBT). Patients were categorised as lactose malabsorption (LM; malabsorption only) or LI [malabsorption plus increase in total symptom score (TSS). Measurements included (i) psychological status; (ii) enteric biopsies with quantification of mast cells (MCs), T-lymphocytes and enterochromaffin cells; (iii) serum cytokines; (iv) rectal sensitivity before and after lactose ingestion. LI was more prevalent in IBS-D patients than HCs [25/55 (46%) vs. 3/18 (17%), P = 0.029]. IBS-D patients with LI had (i) higher levels of anxiety than those with LM (P = 0.017) or HCs (P = 0.006); (ii) increased mucosal MCs compared with LM (P = 0.006) and HCs (P < 0.001); (iii) raised serum TNF-α compared with LM (P = 0.034) and HCs (P < 0.001) and (iv) increased rectal sensitivity after lactose ingestion compared with LM (P < 0.001) or HCs (P < 0.001). Severity of abdominal symptoms after lactose ingestion was associated with the increase in visceral sensitivity after lactose intake (r = 0.629, P < 0.001), MCs (r = 0.650, P < 0.001) and anxiety (r = 0.519, P < 0.001). IBS-D patients with lactose intolerence are characterised by anxiety, mucosal immune activation and increased visceral sensitivity after lactose ingestion. The presence of these biomarkers may indicate an IBS phenotype that responds to dietary therapy and/or mast cell stabilisers (ClinicalTrials.gov Identifier: NCT01286597).Alimentary Pharmacology & Therapeutics 12/2013; · 4.55 Impact Factor