Crohn’s disease (CD) and ulcerative colitis (UC) are chronic, relapsing, inflammatory disorders of the digestive tract that characteristically develop in adolescence and early adulthood. The reported prevalence of malnutrition in inflammatory bowel disease (IBD) patients ranges between 20% and 85%. Several factors, including reduced oral food intake, malabsorption, chronic blood and proteins loss, and intestinal bacterial overgrowth, contribute to malnutrition in IBD patients. Poor nutritional status, as well as selective malnutrition or sarcopenia, is associated with poor clinical outcomes, response to therapy and, therefore, quality of life. The nutritional assessment should include a dietetic evaluation with the assessment of daily caloric intake and energy expenditure, radiological assessment, and measurement of functional capacity.
In recent years, research has focused on the use of dietary fibers and prebiotics, since many of these polysaccharides can be metabolized by intestinal microbiota, leading to the production of short-chain fatty acids. The metabolites of prebiotic fermentation also show anti-inflammatory and immunomodulatory capabilities, suggesting an interesting role in the treatment of several pathological conditions. Galacto-oligosaccharide and short- and long-chain fructans (Fructo-oligosaccharides and inulin) are the most studied prebiotics, even if other dietary compounds seem to show the same features. There is an increasing interest in dietary strategies to modulate microbiota. The aim of this review is to explore the mechanisms of action of prebiotics and their effects on the principal gastro-intestinal disorders in adults, with a special focus on Galacto-oligosaccharides, Fructo-oligosaccharides, lactulose and new emerging substances which currently have evidence of prebiotics effects, such as xilooligosaccharides, soybean oligosaccharides, isomaltooligosaccharides, lactobionic acid, resistant starch and polyphenols.
1 March 2005 in American Journal of Gastroenterology
Summary: Background: The majority of patients with gastro‐oesophageal reflux disease do not present with erosive oesophagitis and make up a heterogeneous group. Patients with non‐erosive gastro‐oesophageal reflux disease are less responsive than patients with oesophagitis to acid‐suppressive therapy.Aim: To assess the role of acid reflux in gastro‐oesophageal reflux disease symptoms.Methods: The spatio‐temporal characteristics of reflux events were analysed and related to reflux perception in 45 patients with non‐erosive gastro‐oesophageal reflux disease and 20 patients with erosive oesophagitis.Results: Compared with healthy controls, all patients showed a higher intra‐oesophageal proximal spread of acid, which was prominent in patients with non‐erosive gastro‐oesophageal reflux disease (> 50% of events lasting for 1–2 min). Irrespective of mucosal injury, the risk of reflux perception was very high when acid reached proximal sensors (odds ratio, 7.6; 95% confidence interval, 4.6–12.5), being maximal in patients with non‐erosive gastro‐oesophageal reflux disease with normal acid exposure time (odds ratio, 11; 95% confidence interval, 5.2–22.3).Conclusions: Patients with non‐erosive gastro‐oesophageal reflux disease are characterized by a significantly higher proportion of proximal acid refluxes and a higher sensitivity to short‐lasting refluxes when compared with patients with oesophagitis. The highest proximal acid exposure and highest perception occurred in patients with non‐erosive gastro‐oesophageal reflux disease presenting with a normal pH‐metric profile. The assessment of acid distribution and its perception in the oesophageal body can better identify reflux patients who should benefit from acid‐suppressive treatment.
The prevalence of obesity is increasing worldwide, leading to a severe impairment of overall health. Actually, obesity has been associated with several pathological conditions, causing an excess overall mortality. In particular, overweight and obesity are well known risk factors for a variety of gastrointestinal (GI) disorders i.e., functional GI disorders as well as, inflammatory bowel disease (IBD), pancreatitis, and GI cancer. The aim of the present review is to summarize the potential role of overweight and obesity in GI disease with particular focus on plausible biological mechanisms that could explain the association between obesity and GI disease based on the most recent evidence in the literature.
8 January 2007 in Alimentary Pharmacology & Therapeutics
Summary: Background Acid exposure of proximal oesophagus and dilated intercellular space diameters of oesophageal epithelium are relevant in the perception of gastro‐oesophageal reflux.Aim To explain the relationship between gastro‐oesophageal reflux disease symptoms, acid exposure and intercellular space diameter along the oesophageal epithelium and to assess time‐related variability of intercellular space diameter.Methods Thirty‐three non‐erosive reflux disease (NERD), six erosive oesophagitis patients and 12 asymptomatic controls underwent oesophageal manometry and 24‐h dual‐channel oesophageal pH‐monitoring following endoscopy. Biopsies were taken 5 cm above the LES and 10 cm below the UES, at comparable levels, as pH sensors. A total of 100 intercellular space diameters per patient/control were measured blindly at transmission electron microscopy. In 15 patients, the investigation was repeated after 1 year.Results In all NERD patients, acid exposure was higher at mid‐proximal oesophagus (P < 0.01) and mean intercellular space diameters, at distal and mid‐proximal oesophagus, was three‐ and twofold higher (1.5 and 0.82 μm, respectively) compared with controls. Intra‐patient intercellular space diameter values were stable over time, not overlapping with those of controls.Conclusions Dilation of intercellular space diameter occurs along the distal and proximal oesophageal epithelium in NERD patients and could be responsible for the enhanced perception of proximal acid reflux. This finding appears to be time‐reproducible and to represent a sensitive, histopathological marker of NERD.