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Background/aims: Steroids have been shown to prevent intestinal oxidative stress. We investigated the effects of methylprednisolone on intestinal oxidative damage and bacterial translocation in thioacetamide-induced liver failure in rats., Materials and Methods: Group 1 (n=8) was the control group. In group 2 (n=8), the thioacetamide group, rats received 300 mg/kg intraperitoneal thioacetamide daily for 2 days. In group 3 (n=8), the thioacetamide+methylprednisolone group, treatment with methylprednisolone (30 mg/kg intraperitoneal) was commenced 48 h before the first dose of thioacetamide. In group 4 (n=8), the methylprednisolone group, the rats received only methylprednisolone (30 mg/kg intraperitoneal)., Results: Serious hepatic and intestinal oxidative damage and high bacterial translocation frequencies were observed in the thioacetamide group compared with those of the controls. Bacterial translocation frequency in the thioacetamide+methylprednisolone group was significantly lower than that in the thioacetamide group (p<0.05). Intestinal thiobarbituric acid-reactive substances and myeloperoxidase levels and tissue damage scores for the intestines in the thioacetamide+methylprednisolone group were lower than those in the thioacetamide group (p<0.01, p<0.01, and p<0.0001, respectively)., Conclusion: Our findings suggest that methylprednisolone reduces bacterial translocation by preventing intestinal oxidative damage in this model of acute liver failure in rats.

Background/aims: Acute pancreatitis is a serious complication of organophosphate poisoning. There is no report in the literature dealing with the development of a pancreatic pseudocyst after complication of organophosphate-induced acute pancreatitis. Therefore, we present a case who developed pancreatic pseudocyst after complication of organophosphate-induced acute pancreatitis., Methods: A 17-year-old female patient with a history of ingestion of complication of organophosphate insecticide (DDVP EC 550, dichlorvos) was admitted with cholinergic symptoms. On admission, serum amylase and lipase levels were high and abdominal ultrasonography showed an edematous pancreas. No etiological factor for acute pancreatitis was evident., Results: We diagnosed complication of organophosphate-induced acute pancreatitis. After four weeks, abdominal abdominal ultrasonography and computerized tomography revealed a pancreatic pseudocyst of 6 cm diameter. During follow-up, the pancreatic pseudocyst size regressed to 4 cm., Conclusion: Complication of organophosphate poisoning can cause acute pancreatitis and its complications. Early diagnosis and appropriate treatment may reduce morbidity and mortality.

Background/aims: Gingko biloba is an antioxidant substance which has antagonistic activity on platelet-activating factor. We aimed to investigate the antioxidant effect and the histopathologic changes caused by Gingko biloba on acetic acid-induced colitis., Methods: Totally 22 rats were divided into three groups. Group 1 (n=7) served as the control group. Group 2 (n=7) and Group 3 (n=8) were given 2 ml/day of 4% acetic acid by intracolonic instillation for three days. Gingko biloba (100 mg/kg) was then given only to Group 3 intraperitoneally for three days. Oxidative stress was assessed by determinate tissue and serum malondialdehyde (MDA) levels, and colonic damage was assessed by histologic examination., Results: Depth of necrosis, extent of necrosis, degree of inflammation, extent of inflammation, fibrosis and total histologic scores in Group 2 were significantly higher than in the control group (p<0.05). The same parameters were lower in Group 3 versus Group 2, but the difference was not significant. Tissue and serum MDA levels in Group 2 were significantly higher than Group 1 (p<0.01 and 0.05, respectively). Again, the same parameters in Group 3 were lower than in Group 2, but the difference was not significant statistically., Conclusions: Gingko biloba did not significantly affect histopathological and oxidative stress parameters in experimental colitis.

Background/aims: Esophageal varices and serum-ascites albumin gradient (SAAG) are two major findings of portal hypertension. Recently, correlation between these two findings in patients with cirrhosis due to alcohol has been attracted attention. We aimed at evaluating whether a correlation exists between these parameters in the patients with non-alcoholic cirrhosis., Methods: Albumin levels in the serum and ascites and esophageal varices were studied and the correlation between these parameters was assessed in 45 patients with non-alcoholic cirrhosis detected between January 2002 and June 2003., Results: Thirty-two of the patients were male and 13 female. The average age of the patients was 56.3+/-12.5 years (range 22-85 years). The causative agents were found to be hepatitis B virus in 35 patients and hepatitis C virus in six patients; no etiology could be determined in the remaining four patients. Serum level of albumin was determined as 2.53+/-0.53 g/dl, ascites level of albumin as 0.42+/-0.31 g/dl and SAAG as 2.1+/-0.51. Endoscopic esophageal examination revealed first-degree esophageal varices in 15 patients, second-degree esophageal varices in 18 patients and third-degree esophageal varices in eight patients; no esophageal varices could be found in four patients. There was no correlation between the degree of the esophageal varices and serum levels of albumin (p=0.7) and SAAG (p=0.2); but a weak correlation was found between the degree of the esophageal varices and ascites levels of albumin (p=0.03, r=0.30). Furthermore, the patients were classified by their SAAG values, and their varices were then assessed. Two of four patients with SAAG values between 1.1 and 1.49 had esophageal varices, as did 13 of 15 patients with SAAG values between 1.5 and 1.99, and all of the patients with SAAG values greater than 2.0., Conclusion: All SAAG values were greater than 1.1 in our non-alcoholic cirrhosis cases. The correlation that has been found to exist between SAAG and esophageal varices could not be found in our patients with non-alcoholic cirrhosis. It is remarkable that most of the patients with non-alcoholic cirrhosis presenting with ascites and all of the patients with an SAAG value greater than 2.0 had esophageal varices.