Methylprednisolone prevents bacterial translocation in thioacetamide-induced liver failure in rats.

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.

Albendazole Induced Recurrent Acute Toxic Hepatitis: A Case Report.

INTRODUCTION: Drug induced acute toxic hepatitis can be idiosyncratic. Albendazole, a widely used broad spectrum antiparasitic drug is generally accepted as a safe drug. It may cause asymptomatic transient liver enzyme abnormalities but acute toxic hepatitis is very rare. Case Report : Herein, we present the case of 47 year old woman with recurrent acute toxic hepatitis after a single intake of albendazole in 2010 and 2014. The patient was presented with symptoms and findings of anorexia, vomiting and jaundice. For diagnosis, other acute hepatitis etiologies were excluded. Roussel Uclaf Causality Assessment Method (RUCAM) score was calculated and found to be 10, which meant highly probable drug hepatotoxicity. Within 2 months, all pathological findings came to normal. RESULT: There are a few reported cases of albendazole induced toxic hepatitis, but at adults, there is no known recurrent acute toxic hepatitis due to albendazole at this certainty according to RUCAM score. CONCLUSION: Physicians should be aware of this rare and potentially fatal adverse effect of albendazole.

Severe hepatitis with prolonged cholestasis and bile duct injury due the long-term use of ornidazole.

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.