Maastricht University Medical Centre and Ferring.

EO IBD is rising, warranting physicians' alertness for IBD in elderly patients. The long-term outcome was not different from AO disease, despite a less frequent use of immunomodulators and biologicals.

The EndoBarrier Gastrointestinal Liner is a feasible and safe noninvasive device with excellent short-term weight loss results. The device also has a significant positive effect on type 2 diabetes mellitus. Long-term randomized and sham studies for weight loss and treatment of diabetes are necessary to determine the role of the device in the treatment of morbid obesity.This study was registered at www.clinicaltrials.gov (registration number: NCT00830440).

Screening for variants in TPMT did not reduce the proportions of patients with hematologic ADRs during thiopurine treatment for IBD. However, there was a 10-fold reduction in hematologic ADRs among variant carriers who were identified and received a dose reduction, compared with variant carriers who did not, without differences in treatment efficacy. ClinicalTrials.gov number: NCT00521950.

Background: Intragastric growth of non‐Helicobacter pylori bacteria commonly occurs during acid‐suppressive therapy. The long‐term clinical consequences are still unclear. Aim: To investigate the luminal and mucosal bacterial growth during gastric acid inhibition, in relation to the type and duration of acid‐inhibitory treatment, as well as to concomitant H. pylori infection. Methods: A total of 145 patients on continuous acid inhibition with either proton pump inhibitors (n=109) or histamine2‐receptor antagonists (H2RAs, n=36) for gastro‐oesophageal reflux disease, and 75 dyspeptic patients without acid inhibition (control group) were included. At endoscopy, fasting gastric juice was obtained for pH measurement and bacteriological culture. Gastric biopsy specimens were examined for detection of H. pylori (immunohistochemistry) and of non‐H. pylori bacteria (modified Giemsa stain‐positive and immunohistochemistry‐negative at the same location). Results: Non‐H. pylori flora was detected in the gastric juice of 92 (41.8%) patients and in the gastric mucosa of 109 (49.6%) patients. In gastric juice, prevalence rate for non‐H. pylori bacteria was higher in patients taking proton pump inhibitors than controls and those taking H2RAs (58.7% vs. 22.6% and vs. 30.6%, P < 0.0001 and P < 0.003, respectively), but did not differ statistically between H2RAs and controls. In gastric mucosa, prevalence rates for non‐H. pylori bacteria were higher in patients taking proton pump inhibitors and H2RAs than in the controls (antrum: 46.9% and 48.6% vs. 25%, P < 0.05 for both; corpus: 52.2% and 56.8% vs. 23.7%, P < 0.001 for both), but did not differ between proton pump inhibitors and H2RAs. Both luminal and mucosal growth of non‐H. pylori bacteria were significantly greater in H. pylori‐positive than ‐negative patients taking proton pump inhibitors (P < 0.05 for both). Luminal growth of non‐H. pylori flora increased with the intragastric pH level, whilst mucosal bacterial growth increased with the duration of acid inhibition. Conclusions: Non‐H. pylori flora not only contaminates the gastric juice but also colonizes the gastric mucosa of a large proportion of patients treated long‐term with acid inhibition. The relationship between H. pylori and non‐H. pylori bacteria in the pathogenesis of atrophic gastritis and gastric cancer needs further elucidation.

Between 1991 and 2014, the hospitalization and surgery rates decreased, whereas progression to complicated disease is still common in CD. These improvements were not significantly related to the use of immunomodulators and biologicals.

During long-term gastric acid inhibition, serum CgA levels reflect the presence and severity of fundic ECL cell hyperplasia. Serum CgA is therefore a useful screening test for gastric ECL cell proliferative changes within this context.

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