HEPATOTOXICITY

Background of Study: Sepsis is characterized by overwhelming surge ofcytokines and oxidative stress to one of many factors, gram negative bacteria being one ofit. Mortality remains very high in septic patients despite the advanced treatments rendered inintensive care units due to multiple organ damage including hepatotoxicity. Study Design:Randomized controlled laboratory trial. Period: 04 months from March 2014-June 2014. Setting:Department of Pharmacology and Therapeutics, Army Medical College, NUST, Rawalpindi.Aim of the Study: The present study was undertaken to learn dexamethasone’s competencein prevention and treatment of LPS/ endotoxin induced hepatotoxicity in mice. Material andMethods: Endotoxin induced hepatotoxicity was reproduced via LPS of serotype E.ColiO111:B4 administrationintraperitoneally at a dose of 10mg/kg and all mice were sacrificed 17hours latters. Dexamethasone (3mg/kg of b.w. i.p) was given 30 minutes before LPS in separateset of animals to determine its preventive role. Whereas therapeutic efficacy was adjudgedby giving dexamethasone 2 hour after LPS administration. Hepatotoxicity was determined byestimation of serum ALT and AST and histopathological analysis of liver sections. Results:LPS administration was associated by statistically elevated serum ALT and AST and markedhepatic inflammation. Dexamethasone was efficacious in a version of LPS induced hepaticdystrophy both when given as pre and post-treatment. Serum ALT and AST were statisticallylower when compared to LPS group. Also hepatic inflammation was statistically lessened bydexamethasone. Conclusion: Low dose dexamethasone has beneficial role in reduction ofLPS/endotoxin induced hepatic injury in experimental model of sepsis.