AIM:To assess the efficacy of intramuscular diclofenac and fluid replacement for prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis. METHODS:A prospective, placebo-controlled study was conducted in 80 patients who underwent ERCP. Patients were randomized to receive parenteral diclofenac at a loading dose of 75 mg followed by the infusion of 5-10 mL/kg per hour isotonic saline over 4 h after the procedure, or the infusion of 500 mL isotonic saline as placebo. Patients were evaluated clinically, and serum amylase levels were measured 4, 8 and 24 h after the procedure. RESULTS:The two groups were matched for age, sex, underlying disease, ERCP findings, and type of treatment. The overall incidence of pancreatitis was 7.5% in the diclofenac group and 17.5% in the placebo group (12.5% in total). There were no significant differences in the incidence of pancreatitis and other variables between the two groups. In the subgroup analysis, the frequency of pancreatitis in the patients without sphincter of Oddi dysfunction (SOD) was significantly lower in the diclofenac group than in the control group (P = 0.047).CONCLUSION: Intramuscular diclofenac and fluid replacement lowered the rate of pancreatitis in patients without SOD.

BackgroundEctopic biliary drainage is a rare congenital anomaly on which we have scarce data in the current literature.MethodsThe data were collected from the records of 400 endoscopic retrograde cholangio-pancreatography (ERCP). In this report, we present 10 cases (male/female: 9/1, mean age 54 years, range 38-74) with ectopic biliary openings into the duodenum and/or stomach diagnosed by endoscopic retrograde cholangio-pancreatography (ERCP).ResultsIn our series, the frequency of ectopic biliary drainage is 2% (10 out of 400 ERCPs). Recurrent attacks of cholangitis and complicated ulcer formation in the distal stomach and bulbar duodenum were the most common signs in the present series. The sites of ectopic biliary drainage were the stomach in 1 case, the duodenum bulbus in 7 cases and the postbulbar duodenum in 2 cases. Bulbar ulcer, deformed pylorus and bulbus were present in 7 cases, apical bulbar stricture in 2, gastric ulcer in 1, pyloroplasty and/or gastroenterostomy in 3 cases. One case had had previous bleeding episode. Some of them had undergone previous surgeries for gall-stone disease (cholecystectomy in 5 cases, bile duct operation in 3 cases) and ulcer complications (pyloroplasty/gastroenterostomy in 3 cases). ERCP revealed dilatation of the biliary tree and hook shaped distal choledochus in all cases, choledocholithiasis in 7 and Mirizzi syndrome in 1. Endoscopic balloon dilatations for gastric outlet obstruction, extraction of bile stones after balloon dilating the ectopic site, surgery for difficult cases with large bile duct stones or with gastric outlet obstruction were preferred methods in this series of patients.ConclusionWith this report, we have to remind that ectopic biliary drainage must be considered in the differential diagnosis when the clinician faces cases with gastric outlet obstruction due to peptic ulcer formation accompanied by cholangitis/cholestasis.

Evidence suggests that gut microbiota dysbiosis plays a critical role in the initiation and promotion of inflammatory bowel disease (IBD). Kefir is a fermented dairy product including yeast and bacterial species. We aimed to investigate the effect of kefir on trinitrobenzene sulfonic acid (TNBS)‐induced colitis in rats using two different doses. Fifty‐four Wistar rats were divided into six groups. For 14 days, the normal control and colitis control groups were given tap water, kefir10 control, kefir10 colitis, and kefir30 control, and the kefir30 colitis groups were given phosphate‐buffered saline containing 10% or 30% kefir, respectively, instead of tap water. Colitis was induced by intracolonically administrating TNBS in the colitis control, kefir10 colitis, and kefir30 colitis groups. On the 14th day, the rats were sacrificed. The weights and lengths of the colons were measured and macroscopically evaluated, and the distal 10 cm segments were subjected to a histopathological examination. The incidence of bloody stool and diarrhea in the kefir10 colitis group was found to be less than the colitis control and kefir30 colitis groups. The colonic weight/length ratio in the kefir10 colitis group was lower than that in the colitis control and kefir30 colitis groups. We detected that the 10% kefir treatment reduced TNBS‐induced macroscopic colonic damage, while it was exacerbated by the 30% kefir treatment. No significant difference was observed between the colitis groups in terms of microscopic colonic damage scoring. These results indicate that kefir, with a careful dose selection, may be a useful agent in the treatment of IBD.

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The protective effect of a probiotic mixture of 13 different bacteria and α-tocopherol on 98% ethanol-induced gastric mucosal injury was evaluated. Levels of gastric mucosal pro- and anti-inflammatory cytokines, malondialdehyde, and secretory immunglobulin A were measured. Rats were allocated into four groups: control, ethanol, probiotic, and α-tocopherol. The control and ethanol groups received skim milk for 14 days. Probiotic and α-tocopherol groups were administered probiotic mixture suspended in skim milk and 100 mg/kg α-tocopherol, respectively, by daily gavage for 14 days. On Day 15, gastric lesions were induced by administration of ethanol 98% (1 mL) to all rats except those in the control group. Probiotic, but not α-tocopherol, seemed to inhibit ethanol-induced gastric mucosal tumor necrosis factor-α, interferon-γ, and interleukin-2 production (P > .05). Ethanol caused the elevation of mucosal interleukin-4 level (compared to the control, P < .05). Probiotic pretreatment significantly suppressed the ethanol-induced increase of gastric mucosal interleukin-4 levels. Pretreatment with either probiotic or α-tocopherol inhibited the ethanol-induced increase of mucosal malondialdehyde concentration (P < .01 and P < .05, respectively). Probiotic pretreatment enhanced the gastric mucosal secretory immunoglobulin A concentration (P < .001). In conclusion, probiotic mixture and α-tocopherol reduced ethanol-induced gastric mucosal lipid peroxidation, suggesting that they may be beneficial for gastric lesions induced by lower ethanol concentration.

Kefir reduces the clinical DAI and histologic colitis scores in a DSS-induced colitis model, possibly via reduction of MPO, TNF-α, and iNOS levels.

Our study suggests that GES with late lung imaging objectively showed the presence of pathologic distal and/or proximal reflux, but rarely pulmonary aspiration, in the majority of chronic cough patients with gastroesophageal reflux disease. As the chronic cough patients with proximal reflux have more severe reflux characteristics, this examination may be effective in screening and following up these patients.