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Nitroimidazole derivatives are commonly used in the treatment of protozoal and anaerobic infections, and reports of their hepatotoxicity are rare. We report a case of severe hepatitis due to the long-term (8 weeks) use of ornidazole. A 27-year-old woman presented for evaluation of elevated serum transaminase and total bilirubin levels. Liver biopsy revealed portal inflammation, hepatocellular and canalicular cholestasis, porto-portal and portocentral bridging fibrosis, and a tendency to form nodules. No aetiological factors associated with chronic liver disease were identified. The abdominal ultrasonographic findings were compatible with chronic liver disease. We therefore made the diagnosis of severe hepatitis resulting from the long-term use of ornidazole. We conclude that nitroimidazole derivatives may lead to serious liver damage, especially in female patients.

WOS: 000273799600004, PubMed ID: 20163034, Background and study aims : Abnormal expression of claudin-4 and beta-catenin play a role in carcinogenesis. The purpose of the present study was to examine claudin-4 and beta-catenin expression in normal and precancerous gastric mucosa. Patients and methods : Endoscopic biopsy specimens [normal gastric mucosa (n = 22), intestinal metaplasia (n = 24), dysplasia (n = 18), Helicobacter pylori (H. pylori)-associated chronic gastritis (n = 32) and remnant gastric mucosa (n = 18)] obtained from different 114 patients were examined by immunohistochemistry. Results : Claudin-4 expression was present in 94.4% of dysplasia, 87.5% of intestinal metaplasia, 62.5% H. pylori-associated chronic gastritis, and 88.9% remnant gastric mucosa but only 18.2% of normal gastric mucosa biopsies. Decreased expression of beta-catenin was present in 27.8% of dysplasia, 8.3% of intestinal metaplasia, 15.6% of H. pylori-associated chronic gastritis, and 22.2% of remnant gastric mucosa biopsies, but was not present in normal gastric mucosa. When compared with normal gastric mucosa, there was a significant difference in claudin-4 expression in all groups (P < 0.05), but a significant difference was detected in dysplasia and remnant gastric mucosa for beta-catenin (P < 0.05). Conclusions : Our results suggest that claudin-4 expression is upregulated in premalignant gastric alterations. (Acta gastroenterol. belg., 2009, 72, 407-412).

Biliary complications are an important cause of mortality and morbidity after living donor liver transplantation (LDLT). We present our endoscopic treatment results after LDLT as a single center with high volume.Patients who underwent endoscopic retrograde cholangiopancreatography (ERCP) after LDLT between 2005 and 2015 were included. Clinical data included patient demographics, ERCP indications (stricture or leak), and treatment outcomes, including need for percutaneous and surgical interventions.ERCP was performed in 446 (39.2%) patients with duct-to-duct anastomosis of 1136 LDLT patients. The most common biliary complication was stricture ± stone (70.6%, 315/446). Stricture and leak occurred in 60 (13.4%) patients. Only biliary leak was found in 40 (8.9%) patients. Our endoscopic treatment success rate in patients with biliary stricture after LDLT was 65.1%. Overall endoscopic success rates in our patients were 55.0% in patients with both leak and stricture, and only leak. In all, our percutaneous transhepatic biliary interventions (PTBI) and ERCP success rate was 90.6% in patients with biliary complications after LDLT.Endoscopic treatments are highly effective for biliary complications after LDLT. Effective use of percutaneous interventions in collaboration with endoscopic treatments significantly reduces the need for surgical treatment.