No abstract

Several risk scoring systems exist for acute upper gastrointestinal bleeding (UGIB). The clinical Rockall score (clinical RS) and the Glasgow Blatchford score (GBS) are major risk scores that consider only clinical data. Computed tomography (CT) findings are equivocal in non variceal UGIB. We compared CT findings with clinical data to predict mortality, rebleeding and need for endoscopic therapy in non variceal UGIB patients. This retrospective, single center study included 386 patients admitted to our emergency depart ment with diagnosis of non variceal UGIB by urgent endoscopy between January 2009 and March 2015. Multivariable logistic regression analysis was used to investigate CT findings and risk factors derived from clinical data. CT findings could not signifi cantly predict mortality and rebleeding in non variceal UGIB patients. However, upper gastrointestinal hemorrhage in CT findings better predicted the need for endoscopic therapy than clinical data. The adjusted odds ratios were 10.10 (95% CI 5.01-20.40) for clinical RS and 10.70 (95% CI 5.08-22.70) for the GBS. UGI hemorrhage in CT findings could predict the need for endo scopic therapy in non variceal UGIB patients in our emergency department. CT findings as well as risk score systems may be useful for predicting the need for endoscopic therapy.

The gastrointestinal effects of α-glucosidase inhibitors have not been sufficiently investigated. The aim of this study was to determine whether a single dose of pre-prandial voglibose might affect the rate of gastric emptying, determined using the 13C breath test. Ten healthy male volunteers participated in this randomized, two-way crossover study. The subjects fasted overnight and received 0.2 mg voglibose or a placebo 2 h before a test meal. They were then served a liquid test meal consisting of 200 kcal per 200 ml that contained 100 mg 13C-acetate. Breath samples were collected under both conditions until 150 min after the meal. A comparison of the control and voglibose conditions revealed that for gastric emptying rates (with values expressed as median: range), T1/2 [(87.9: 78.0–104.9 min) vs (88.4: 74.3–106.3 min), p = 1], Tlag [(47.1: 39.6–60.1 min) vs (45.4: 31.2–63.3 min), p = 0.432], β [(1.89: 1.68–2.18) vs (1.90: 1.35–2.15), p = 0.846] and κ [(0.81: 0.71–0.98) vs (0.81: 0.50–0.94), p = 0.922] did not significantly differ between conditions. A significant difference between the control and voglibose conditions was found for the GEC [(4.28: 4.09–4.44) vs (4.06: 3.69–4.50), p = 0.0138]. In conclusion, this study demonstrated that the ingestion of oral voglibose led to delayed gastric emptying of a liquid meal.

The effects of acotiamide on gastrointestinal motility have not been sufficiently investigated. The aim of this study was to determine whether single preprandial acotiamide or mosapride intake might affect the gastric emptying rate using the 13 C breath test. Here, 11 healthy volunteers participated in a randomized three-way crossover study. The subjects received acotiamide (100 mg) or mosapride (5 mg) or placebo before liquid test meal ingestion. Gastric emptying was estimated by determining following parameters: the time required for 50% emptying of the labeled meal (T1/2), lag time for 10% emptying of the labeled meal (Tlag), gastric emptying coefficient (GEC) and regression-estimated constants (β and κ). These parameters were calculated from a 13 CO 2 breath excretion curve using conventional formulas. The acotiamide, mosapride and placebo conditions were compared, revealing that for gastric emptying rates (values expressed as median), T1/2 (87.83571 min vs 79.95057 min vs 88.74378 min, p = 0.1496), Tlag (46.36449 min vs 42.2897 min vs 47.08094 min, p = 0.4966), GEC (4.382027 vs 4.211441 vs 4.248495, p = 0.8858), β (1.917728 vs 1.757062 vs 1.869141, p = 0.4066) and κ (0.834051 vs 0.819820 vs 0.789523, p = 0.1225) did not significantly differ. In this study, acotiamide (100 mg) or mosapride (5 mg) had no effect on gastric emptying.

BackgroundAn ideal medication for acid-related diseases would offer prompt stopping of blood flow as well as efficient symptom resolution. The aim of this study was to investigate the gastric acid suppression potency of a single oral dose of rabeprazole alone, compared with administration of rabeprazole plus mosapride.MethodsTwelve male volunteers, Helicobacter pylori (H. pylori)-negative, participated in this randomized, three-way crossover study. After a single oral administration of rabeprazole, rabeprazole with mosapride, or rabeprazole administered 1 h after mosapride, we monitored their intragastric pH constantly for 6 h. A 7-day washout period was allowed between each administration.ResultsThe median 6-h intragastric pH after the administration of rabeprazole 1 h after mosapride was 4.41±1.22 (mean±s.d.), significantly higher than after rabeprazole alone 3.45±1.33, P=0.0376). There was no significant difference between the median 6-h pH after the administration of rabeprazole plus mosapride and that after rabeprazole alone (3.81±0.98 vs. 3.45±1.33, respectively; P=0.0927).ConclusionAn oral dose of rabeprazole administered 1 h after mosapride increased the intragastric pH more rapidly than rabeprazole alone, in healthy, male, H. pylori-negative volunteers.