The role of simeticone in small-bowel preparation for capsule endoscopy.

BACKGROUND AND STUDY AIMS: Capsule endoscopy is a new diagnostic method allowing painless visualization of the entire small bowel. However, there is as yet no standardized protocol for bowel preparation before the examination. The aim of this study was to assess the effectiveness of simeticone in reducing bowel gas bubbles in patients undergoing capsule endoscopy. PATIENTS AND METHODS: A randomized, prospective, and controlled study was conducted, including 56 patients, from March to October 2004. The patients were randomly allocated to groups receiving either simeticone or no simeticone, on the basis of a computer-generated random number table. Patients in the simeticone group (n = 28) received 300 mg simeticone for bowel preparation 20 min before capsule endoscopy, while patients in the non-simeticone group (n = 28) received no medication for bowel preparation. Two experienced endoscopists assessed and graded the visibility of the mucosa and intraluminal gas bubbles in a single-blinded fashion. RESULTS: The visibility of the mucosa in the proximal small bowel in patients who received preparation with simeticone was considered to be better, with fewer intraluminal bubbles, than in those without bowel preparation ( P < 0.025). Interobserver agreement was excellent ( R > or = 0.8, P < 0.05). No adverse effects of simeticone were observed. CONCLUSIONS: Simeticone administration before capsule endoscopy improves the visualization of the mucosa in the proximal small intestine.

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis.

BACKGROUND: Gastrin G cells and somatostatin D cells are important regulators of gastric acid secretion and alterations in their relative numbers may play a key role in gastroduodenal disease. AIM: To investigate the effect of Helicobacter pylori infection on the density of immunoreactive G and D cells in gastric antral and corpus biopsies from patients with dyspeptic complaints. METHODS: One hundred and twenty two patients with dyspeptic complaints had two antrum and two corpus biopsies taken during upper endoscopy. The severity of inflammation and the density of H pylori were evaluated semiquantitatively. In addition, the density and distribution of neuroendocrine cells, especially G and D cells, were examined using immunohistochemistry. Patients were divided into three groups, those with H pylori positive gastritis, H pylori negative gastritis, and histologically normal gastric mucosa. RESULTS: The number of immunoreactive G cells was significantly higher and the number of immunoreactive D cells lower in patients with H pylori positive gastritis compared with H pylori negative gastritis or histological normal gastric mucosa. The percentage of G cells as a percentage of mucosal endocrine cells was also raised and that of D cells was decreased. CONCLUSIONS: Helicobacter pylori infection produces alterations in the number of endocrine cells responsible for regulating acid secretion in relation to intragastric pH and feeding. The alterations correlate best with the severity of inflammation and not with H pylori density.