Background /PurposeLimited data are available for acute cholecystitis after Self‐Expandable Metallic Stent (SEMS) placement in patients with malignant distal biliary obstruction. We aimed to identify risk factors for cholecystitis.MethodsThis was a retrospective, single‐center study of 280 patients (336 stents) who received endoscopic SEMS placement between May 2005 and April 2016. Clinical records were used to perform risk factor analyses.ResultsOf 336 SEMS placement procedures, 25 (7.4%) led to development of cholecystitis. Logistic regression analysis revealed three independent risk factors: covered SEMS (P = .014), tumor involvement to the cystic duct (P = .017), and presence of gallstones (P = .022). Median time to cholecystitis onset was shorter with covered SEMS than with uncovered SEMS (P = .034), and in patients with pancreatic cancer compared to those with other cancers (P = .001). Severe cholecystitis developed within 30 days after covered SEMS placement in three patients with pancreatic cancer without tumor involvement to the cystic duct.ConclusionsUse of covered SEMS might be a risk factor for cholecystitis onset within 30 days after placement. Clinicians should be aware of the risk for severe cholecystitis after covered SEMS placement, even if the tumor does not invade the cystic duct.

Background and Aim: Healing speed of peptic ulcer is affected by a number of factors, including Helicobacter pylori (H. pylori) infection and intragastric pH. Acid inhibition exerted by proton pump inhibitors differs by CYP2C19 genotype. Herein, we investigated whether healing speed of artificial ulcers formed after endoscopic submucosal dissection (ESD) was influenced by H. pylori infection, CYP2C19 genotype, or other factors.Methods: A total of 96 H. pylori-positive patients with gastric tumors scheduled for ESD were randomly assigned to receive eradication therapy for H. pylori before ESD (pre-ESD eradication) (n = 44) or after (post-ESD eradication) (n = 52). Patients received eradication therapy consisting of lansoprazole 30 mg, amoxicillin 750 mg, and clarithromycin 200 mg twice daily for 1 week. After ESD, lansoprazole 30 mg was given once daily for 8 weeks. Ulcer size was endoscopically measured on the next day and at 4 and 8 weeks after ESD.Results: Mean reduction rate of artificial ulcer area in the pre-ESD eradication group was 94.7% ± 5.5% at 4 weeks, which was similar to that in the post-ESD eradication group (94.7% ± 6.7%, P = 0.987), irrespective of CYP2C19 genotype. In multivariate analyses, location of gastric tumor (middle and upper, odds ratio: 4.05, 95% CI: 1.620-10.230, P = 0.003) was a factor for 97% reduction of artificial ulcer area at 4 weeks post-ESD, but CYP2C19 genotype and H. pylori infection were not. Conclusion:Healing speed of ESD-induced artificial ulcer was affected by tumor location, but not by time of H. pylori eradication, resected size, or CYP2C19 genotype.

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Endoscopic submucosal dissection (ESD) is a novel endoscopic procedure first developed in the 1990s which enables en bloc resection of gastric neoplastic lesions that are difficult to resect via conventional endoscopic mucosal resection. However, given that ESD increases the risk of intra- and post-ESD delayed bleeding and that platelet aggregation and coagulation in artificial ulcers after ESD strongly depend on intragastric pH, faster and stronger acid inhibition via proton pump inhibitors (PPIs) and histamine 2-receptor antagonists (H2RAs) as well as endoscopic hemostasis by thermocoagulation during ESD have been used to prevent ESD-related bleeding. Because PPIs more potently inhibit acid secretion than H2RAs, they are often the first-line drugs employed in ESD treatment. However, acid inhibition after the initial infusion of a PPI is weaker in the early phase than that achievable with H2RAs; further, PPI effectiveness can vary depending on genetic differences in CYP2C19. Therefore, optimal acid inhibition may require tailored treatment based on CYP2C19 genotype when ESD is performed, with a concomitant infusion of PPI and H2RA possibly most effective for patients with the rapid metabolizer CYP2C19 genotype, while PPI alone may be sufficient for those with the intermediate or poor metabolizer genotypes.

BackgroundMesenteric inflammatory veno-occlusive disease (MIVOD) is difficult to diagnose because of its rarity, nonspecific clinical findings, and frequent confusion with other diseases including inflammatory bowel disease. This report presents a very rare case of MIVOD that occurred during the course of ulcerative colitis (UC).Case presentationA 32-year-old man, who had been diagnosed with UC at the age of 29 and was in remission maintained by oral administration of 5-aminosalicylic acid (5-ASA), showed exacerbation of diarrhea and was admitted to the hospital. Since it was deemed an exacerbation of UC, intravenous steroid therapy and oral administration of tacrolimus were initiated, but his condition continued to worsen. Abdominal computed tomography (CT) was performed and showed intraperitoneal free air, leading to a diagnosis of gastrointestinal perforation and the performance of emergency surgery (subtotal colectomy and ileostomy). Histopathological examination of the resected colon of the patient showed mucosal inflammatory findings that were not typical of UC, including multiple organized thrombi with recanalization in the veins existing in the submucosal layer to the subserosal layer and an increased infiltration of inflammatory cells. These findings led to the pathological diagnosis of MIVOD.ConclusionWe report a very rare case in which MIVOD occurred during the course of UC.