Telemedicine for management of inflammatory bowel disease (myIBDcoach): a pragmatic, multicentre, randomised controlled trial

Cellular mechanisms in basic and clinical gastroenterology and hepatolog

Novel Perceived Stress and Life Events Precede Flares of Inflammatory Bowel Disease: A Prospective 12-Month Follow-Up Study

Cellular mechanisms in basic and clinical gastroenterology and hepatolog

Review article: The diagnosis and management of gastroparesis

BACKGROUND: Gastroparesis is a disorder characterized by a delay in gastric emptying of a meal in the absence of a mechanical gastric outlet obstruction. AIM: To provide an evidence based overview on diagnosis and management of gastroparesis. METHODS: A PubMed search was performed using search terms including gastroparesis, gastric retention, gastric emptying, accommodation, manometry, prokinetics, antiemetics, metoclopramide, domperidone, erythromycin, botulinum toxin, gastric pacing. Relevant studies were identified and original articles and reviews were collected. References in these articles were examined for relevance and included where appropriate. RESULTS: Diagnosis of gastroparesis is based on the presence of symptoms such as nausea, vomiting and postprandial abdominal fullness and on an objectively determined delay in gastric emptying. The true prevalence of gastroparesis is unknown. Gastric emptying can be assessed by scintigraphy and stable isotope breath tests. Management of gastroparesis consists of dietary and lifestyle measures and/or pharmacological interventions (prokinetics, antiemetics, intrapyloric botulinum toxin injection) or other interventions that focus on adequate nutrient intake either through a nasoduodenal tube, percutaneous gastrostomy or jejunostomy. CONCLUSIONS: Accurate diagnosis of gastroparesis requires an adequate protocol to measure gastric emptying. Treatment options in gastroparesis remain limited despite the disabling nature of the disorder

Increased proton pump inhibitor and NSAID exposure in irritable bowel syndrome: results from a case-control study

BACKGROUND: Patients with irritable bowel syndrome (IBS) seen by a gastroenterologist often utilize medications that may alter intestinal homeostasis. The question arises whether exposure to these drugs is associated with the development of IBS symptoms. Aim of this study was therefore to assess the use of PPIs and NSAIDs in patients with IBS versus controls. METHODS: Cases of IBS from the last 5 years were reviewed. All patients having had at least one prescription for a particular drug (PPIs, NSAIDs, SSRIs, diuretics, ACE inhibitors) in the 6 months prior to the time of initial symptom onset were considered exposed. The control group consisted of individuals randomly selected from the general population. RESULTS: 287 cases of IBS were retrieved for analysis together with 287 age and sex-matched controls. Exposure to PPIs and NSAIDs was significantly higher in IBS patients, whereas no association between ACE inhibitor use and IBS was found. PPIs were not significantly associated when excluding patients with gastrointestinal reflux disease or functional dyspepsia. Exposure to SSRIs was also positively associated with IBS, but only when patients with psychiatric comorbidity were included in the analyses. CONCLUSIONS: Medications that may alter intestinal homeostasis such as NSAIDs and PPIs were more frequently used in IBS patients compared to controls. This association might be relevant for everyday clinical practice, but it is remains to be elucidated whether this association is of etiological nature

Review article: The gastrointestinal tract: neuroendocrine regulation of satiety and food intake

BACKGROUND: The gastrointestinal tract elicits numerous signals regulating food intake and satiety, and recently many studies have been performed to elucidate the mechanisms regulating these signals. AIM: To describe the effects of the gastrointestinal tract on satiety, satiation and food intake. METHODS: A PubMed search was performed to identify and select the relevant literature using search terms including 'gastric satiety, intestine + satiety, satiation, cholecystokinin, ghrelin, peptide YY, glucagon-like peptide-1 and ileal brake'. RESULTS: Satiation, satiety and food intake result, among other factors, from signals originating in the stomach caused by distension and signals from the small intestine. These intestinal signals result from nutrient sensing in the gut and activate neural and humoral pathways. Activation of the distal part of the gut, the so called ileal brake, leads to reduction in hunger and food intake, and models of chronic ileal brake activation lead to massive weight loss. CONCLUSION: Gastrointestinal signals are crucial for the regulation of food intake, satiety and satiation. The ileal brake deserves special attention, as both ileal intubation studies and surgical studies demonstrate that activation of the ileal brake reduces food intake. In the surgical models, weight loss occurs without adaptation to the anorectic effects of ileal brake activation

Ethanol metabolism and its effects on the intestinal epithelial barrier

Ethanol is widely consumed and is associated with an increasing global health burden. Several reviews have addressed the effects of ethanol and its oxidative metabolite, acetaldehyde, on the gastrointestinal (GI) tract, focusing on carcinogenic effects or alcoholic liver disease. However, both the oxidative and the nonoxidative metabolites of ethanol can affect the epithelial barrier of the small and large intestines, thereby contributing to GI and liver diseases. This review outlines the possible mechanisms of ethanol metabolism as well as the effects of ethanol and its metabolites on the intestinal barrier. Limited studies in humans and supporting in vitro data have indicated that ethanol as well as mainly acetaldehyde can increase small intestinal permeability. Limited evidence also points to increased colon permeability following exposure to ethanol or acetaldehyde. In vitro studies have provided several mechanisms for disruption of the epithelial barrier, including activation of different cell-signaling pathways, oxidative stress, and remodeling of the cytoskeleton. Modulation via intestinal microbiota, however, should also be considered. In conclusion, ethanol and its metabolites may act additively or even synergistically in vivo. Therefore, in vivo studies investigating the effects of ethanol and its byproducts on permeability of the small and large intestines are warranted