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Background and Aim The endoscopic retrograde cholangiopancreatography (ERCP) procedure is generally performed in patients with high comorbidity. We aimed to reduce the consumption of propofol by adding lidocaine before ERCP. Methods Eighty ERCP patients with ASA I–III, aged between 45–75 years, were randomly divided into two groups. Lidocaine group (group L, n = 40), received 1‐mg midazolam, 1.5 mg/kg lidocaine, and 1 mg/kg propofol intravenously. The control group (group C, n = 40) received 1‐mg midazolam, saline in the same volume as the lidocaine group, and 1 mg/kg propofol intravenously. Propofol was administered with intermittent bolus doses. Propofol consumption, oropharyngeal reflex, recovery time, endoscopist satisfaction, ketamine need, and side‐effects were recorded. Results Propofol consumption during the procedure was statistically lower in group L than in the control group (157.25 ± 39.16 mg vs 228.75 ± 64.62 mg respectively, P < 0.001). Additionally, recovery time was statistically faster in group L compared with the control group (7.78 ± 3.95 min vs 11.92 ± 3.24 min respectively, P < 0.001). The oropharyngeal reflex was less in group L than control group (6/40 vs 15/40 respectively, P = 0.042). There was no significant difference between the two groups regarding visual analogue scale scores and endoscopist satisfaction (P > 0.05). Conclusions We recommend the use of intravenous lidocaine before the ERCP procedure as it reduces propofol consumption, recovery times, and oropharyngeal reflex.

Background Aim. In case of high-dose acetaminophen intake, the active metabolite can not bind to the glutathione, thereby inducing cellular necrosis through binding to the cytosol proteins. This trial was performed to histologically and biochemically investigate whether leptin was protective against liver damage induced by paracetamol at toxic doses. Material and Method. In our trial, 30 female rats, divided into 5 groups, were used. IP leptin administration was performed after an hour in the group of rats, in which paracetamol poisoning was induced. The groups were as follows: Group 1: the control group, Group 2: 20 µg/kg leptin, Group 3: 2 g/kg paracetamol, Group 4: 2 g/kg paracetamol + 10 µg/kg leptin, and Group 5: 2 g/kg paracetamol + 20 µg/kg leptin. Results. The most significant increase was observed in the PARA 2 g/kg group, while the best improvement among the treatment groups occurred in the PARA 2 g/kg + LEP 10 µg/kg group (p < 0.05). While the most significant glutathione (GSH) reduction was observed in the PARA 2 g/kg group, the best improvement was in the PARA 2 g/kg + LEP 10 µg/kg group (p < 0.05). Conclusion. Liver damage occurring upon paracetamol poisoning manifests with hepatocyte breakdown occurring as a result of inflammation and oxidative stress. Leptin can prevent this damage thanks to its antioxidant and anti-inflammatory efficacy.

Background & aims Ulcerative colitis (UC) is an inflammatory bowel disease characterized by mucosal inflammation. Endocan, a proteoglycan secreted by endothelial cells in response to inflammatory cytokines, has been reported to be overexpressed in inflammatory conditions. In this study, we aimed to evaluate the utility of endocan level in determining the extent and severity of disease in patients with ulcerative colitis and to determine whether it can be a candidate marker for noninvasive evaluation and monitoring since there is not enough data in the literature. Materials and methods Sixty-five people were included in the study, including thirty-five with ulcerative colitis and thirty in the control group. Patients with first diagnosed ulcerative colitis clinically, endoscopically, and histopathologically, without any treatment, and with normal liver and kidney tests were included in the study. Endoscopic scoring of all patients was performed according to the Mayo endoscopic scoring (MES) system. Blood samples for CRP (C-reactive protein) and endocan were taken from the patients simultaneously. Results There was a significant statistical difference between all patients with ulcerative colitis and the control group in both endocan level and CRP level (p < 0.001). There was a statistically significant difference between endocan levels and CRP levels between the left-distal group and pancolitis (diffuse colitis) patients, but there was no statistical difference between age and MES. Conclusion Serum endocan level can be useful in determining the extent of ulcerative colitis and planning treatment.